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Endothelial and epithelial barrier dysfunction due to increased permeability and heightened inflammatory reactions influences the emergence of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Nevertheless, bibliometric research comparing endothelial and epithelial barriers is limited. Therefore, this bibliometric study analyzed the Web of Science Core Collection (WoSCC) of the Science Citation Index Expanded literature to explore present research priorities and development tendencies within this field. We conducted a comprehensive search (October 18, 2023) on WoSCC from January 1, 2010, to October 18, 2023, focusing on articles related to endothelial and epithelial barriers in ALI and ARDS. Retrieved data were visualized and analyzed using R-bibliometrix, VOS viewer 1.6.19, and CiteSpace 6.2. R4. Functional enrichment analysis of gene targets identified in the keyword list using Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene ontology databases, and based on the STRING database to construct a PPI network to predict core genes. A total of 941 original articles and reviews were identified. The United States had the highest number of publications and citations and the highest H-index and G-index. According to the Collaboration Network Analysis graph, the United States and China had the strongest collaboration. Birukova AA had the most publications and citations among all authors, while eight of the top ten institutions with mediator centrality were located in the United States. The American Journal of Physiology-Lung Cellular and Molecular Physiology was the leading journal and had the most well-established publication on endothelial and epithelial barriers in ALI and ARDS. Bibliometric analysis revealed that the most frequently used keywords were acute lung injury, ARDS, activation, expression, and inflammation. RHOA appeared most frequently among gene-related keywords, and the PI3K-AKT signaling pathway had the highest count in KEGG pathway enrichment. Research on endothelial versus epithelial barriers in ALI and ARDS remains preliminary. This bibliometric study examined cooperative network connections among countries, authors, journals, and network associations in the cited references. Investigation of the functions of the endothelial and epithelial barriers in ALI/ARDS associated with COVID-19 has recently gained significant attention.

The rat estrous cycle first characterized by Long and Evans in 1922 profoundly affected the course of endocrine research. Investigators took advantage of sex steroid hormone fluctuations associated with the cycle to assess hormonal influences on anxiety, depression, food intake, stress, brain structure and other traits. Similarities of the rat estrous and human menstrual cycles facilitated understanding of human reproductive physiology. I assessed the impact of awareness of the estrous cycle on the emergence of a sex bias that excluded female rats from biomedical research. Beginning with the 1918 volume of the American Journal of Physiology and ending in 1976 when the journal subdivided into several separate disciplinary journals, all studies conducted on rats were downloaded; the use of females, males, both sexes and sex left unspecified was tabulated for 485 articles. A second analysis tracked the number of rat estrous cycle studies across all disciplines listed in PubMed from 1950 to 2021. The description and awareness of variability associated with the rat estrous cycle was correlated with a precipitous decline in investigations that incorporated both sexes, a marked increase in male-only studies and a striking sex bias that excluded female rats. The number of rat estrous cycles studies increased markedly from earlier decades to a peak in 2021. The initial description the rat estrous cycle was correlated with a substantial decline in investigations that incorporated both sexes; one result was a marked increase in male-only studies and a striking sex bias that excluded female rats from biomedical research. Recognition of the advantages of studies that incorporate the rat estrous cycle has resulted in recent years in an increase of such investigations. Female rats and females of several other species are not more variable than their male counterparts across traits, arguing for female inclusion without requiring cycle monitoring. There, remain, however, many advantages of incorporating the estrous cycle in contemporary research.

Cerebral microhemorrhages (CMHs, microbleeds), a manifestation of age-related cerebral small vessel disease, contribute to the pathogenesis of cognitive decline and dementia in older adults. Histological studies have revealed that CMHs exhibit distinct morphologies, which may be attributed to differences in intravascular pressure and the size of the vessels of origin. Our study aimed to establish a direct relationship between the size/morphology of CMHs and the size/anatomy of the microvessel of origin. To achieve this goal, we adapted and optimized intravital two-photon microscopy-based imaging methods to monitor the development of CMHs in mice equipped with a chronic cranial window upon high-energy laser light-induced photodisruption of a targeted cortical arteriole, capillary, or venule. We assessed the time course of extravasation of fluorescently labeled blood and determined the morphology and size/volume of the induced CMHs. Our findings reveal striking similarities between the bleed morphologies observed in hypertension-induced CMHs in models of aging and those originating from different targeted vessels via multiphoton laser ablation. Arteriolar bleeds, which are larger (>&#x2009;100&#xa0;&#x3bc;m) and more widely dispersed, are distinguished from venular bleeds, which are smaller and exhibit a distinct diffuse morphology. Capillary bleeds are circular and smaller (<&#x2009;10&#xa0;&#x3bc;m) in size. Our study supports the concept that CMHs can occur at any location in the vascular tree, and that each type of vessel produces microbleeds with a distinct morphology. Development of CMHs resulted in immediate constriction of capillaries, likely due to pericyte activation and constriction of precapillary arterioles. Additionally, tissue displacement observed in association with arteriolar CMHs suggests that they can affect an area with a radius of&#x2009;~&#x2009;50&#xa0;&#x3bc;m to&#x2009;~&#x2009;100&#xa0;&#x3bc;m, creating an area at risk for ischemia. Longitudinal imaging of CMHs allowed us to visualize reactive astrocytosis and bleed resolution during a 30-day period. Our study provides new insights into the development and morphology of CMHs, highlighting the potential clinical implications of differentiating between the types of vessels involved in the pathogenesis of CMHs. This information may help in the development of targeted interventions aimed at reducing the risk of cerebral small vessel disease-related cognitive decline and dementia in older adults.

Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are common and critical pulmonary conditions involving numerous inflammatory factors and oxidative stress responses. Inflammatory responses and oxidative stress are closely related to the development of ALI/ARDS and form an important theoretical basis for treatment and drug development. Although there has been extensive research on the resolution of inflammation in ALI/ARDS, no systematic bibliometric analysis has been conducted in this field. The researchers used bibliometrics to search the Web of Science Core Collection (WOSCC) database for research literature on the resolution of inflammation in ALI/ARDS from 2005 to 2024. Visualization mapping analysis was performed using tools such as CiteSpace and VOSviewer to analyze authors, research institutions, countries, journals, cocited literature, and keywords. A total of 375 articles were included. The research showed an upward trend, with the highest number of publications in 2022. The United States took the leading position in this field, followed by China. JIN SW had the highest number of publications, while D'Alessio FR had the highest citation count. Harvard University had the highest intermediary centrality, the American Journal of Physiology-Lung Cellular and Molecular Physiology published the most articles, and the American Journal of Respiratory and Critical Care Medicine had the highest impact factor. Resolvin D1 (RvD1) and Resolvin E1 (RvE1) played a key role in the resolution of inflammation. Drug delivery systems (DDSs), such as black phosphorus nanosheets (BPNSs) and liposomes, could efficiently deliver these mediators to enhance therapeutic effects and reduce side effects. Over the past 20 years, interest in the resolution of inflammation in ALI/ARDS has grown. The United States has dominated research in this area. The study of RvD1 and RvE1 has become a hot topic, and the development of DDSs has provided new strategies for clinical treatment.

It was an honor to be asked to deliver the Walter B. Cannon Lecture during the 2024 American Physiological Summit meeting. Dr. Cannon served as president of the American Physiological Society from 1914-1916. He coined the term "fight or flight" to describe an animal's response to threats and the concept of Homeostasis. He was the consummate physician-scientist, an outstanding mentor and teacher, a prolific writer, and a humanitarian. The title of my lecture is based on a poem entitled "Ithaca," written by the Greek poet C. P. Cavafy, who recounts the 10 yr travels of Ulysses, from Troy to his home, Ithaca. Odysseus had to overcome many obstacles to survive this long journey. Like Odysseus, I encountered myriad of professional and health problems. But, I also have experienced the thrill of contributing to scientific knowledge, the satisfaction of watching my mentees develop into independent scientists, the excitement of teaching respiration physiology to medical and professional students, and the pleasure of being of service to my discipline by serving as Editor of the American Journal of Physiology-Lung Cellular and Molecular Physiology and of Physiological Reviews. During my career, I have been interested in identifying the basic mechanisms by which oxidant gases and pathogens damage the blood gas barrier resulting in acute and chronic lung injury. In this brief review, I summarize the results of current studies implicating free heme as a major mediator of acute lung injury and our efforts to develop recombinant forms of human hemopexin, as a countermeasure.

Background: Renal repair is closely related to the prognosis of acute kidney injury (AKI) and has attracted increasing attention in the research field. However, there is a lack of a comprehensive bibliometric analysis in this research area. This study aims at exploring the current status and hotspots of renal repair research in AKI from the perspective of bibliometrics. Methods: Studies published between 2002 and 2022 related to kidney repair after AKI were collected from Web of Science core collection (WoSCC) database. Bibliometric measurement and knowledge graph analysis to predict the latest research trends in the field were performed using bibliometrics software CiteSpace and VOSviewer. Results: The number of documents related to kidney repair after AKI has steadily increased over 20 years. The United States and China contribute more than 60% of documents and are the main drivers of research in this field. Harvard University is the most active academic institution that contributes the most documents. Humphreys BD and Bonventre JV are the most prolific authors and co-cited authors in the field. The American Journal of Physiology-Renal Physiology and Journal of the American Society of Nephrology are the most popular journals in the field with the greatest number of documents. "exosome", "macrophage polarization", "fibroblast", and" aki-ckd transition" are high-frequency keywords in this field in recent years. Extracellular vesicles (including exosomes), macrophage polarization, cell cycle arrest, hippo pathway, and sox9 are current research hotspots and potential targets in this field. Conclusion: This is the first comprehensive bibliometric study on the knowledge structure and development trend of AKI-related renal repair research in recent years. The results of the study comprehensively summarize and identify research frontiers in AKI-related renal repair.

Diabetic Cardiomyopathy (DCM) is a distinct form of heart disease whose pathogenesis remains largely elusive. Recent studies have shed light on the significant role of mitochondria in the development of DCM, emphasizing their critical involvement. Despite these advancements, a bibliometric analysis focusing on the nexus between mitochondria and DCM has not been conducted, leaving a gap in a holistic understanding of research trends in this field. This study extracted publications addressing the role of mitochondria in DCM from the Web of Science Core Collection, spanning from 1988 to 2024. A detailed bibliometric analysis was undertaken using tools like CiteSpace, VOSviewer, Microsoft Excel, and Tableau Public to assess the data. The analysis encompassed 440 publications involving 2705 researchers from 1457 institutions across 175 countries/regions. These studies were disseminated across 202 journals. China was the most prolific country with 192 publications, followed by the United States with 156, and Canada with 26. E. Dale Abel emerged as the most prolific author in this area. Key journals contributing to this research included the American Journal of Physiology-Heart and Circulatory Physiology and the Journal of Molecular and Cellular Cardiology. The future research direction is likely to focus deeper into the mechanisms of mitochondrial dysfunction in the diabetic heart and to identify molecular and cellular targets for therapeutic intervention. This report presents the first detailed bibliometric review of the intersection between mitochondrial research and DCM. It offers critical insights and guidance for researchers aiming to navigate and contribute to this evolving area of study.

High K+ supplementation is correlated with a lower risk of the composite of death, major cardiovascular events, and ameliorated blood pressure, but the exact mechanisms have not been established. Inwardly rectifying K+ (Kir) channels expressed in the basolateral membrane of the distal nephron play an essential role in maintaining electrolyte homeostasis. Mutations in this channel family have been shown to result in strong disturbances in electrolyte homeostasis, among other symptoms. Kir7.1 is a member of the ATP-regulated subfamily of Kir channels. However, its role in renal ion transport and its effect on blood pressure have yet to be established. Our results indicate the localization of Kir7.1 to the basolateral membrane of aldosterone-sensitive distal nephron cells. To examine the physiological implications of Kir7.1, we generated a knockout of Kir7.1 (Kcnj13) in Dahl salt-sensitive (SS) rats and deployed chronic infusion of a specific Kir7.1 inhibitor, ML418, in the wild-type Dahl SS strain. Knockout of Kcnj13 (Kcnj13-/-) resulted in embryonic lethality. Heterozygous Kcnj13+/- rats revealed an increase in K+ excretion on a normal-salt diet but did not exhibit a difference in blood pressure development or plasma electrolytes after 3 wk of a high-salt diet. Wild-type Dahl SS rats exhibited increased renal Kir7.1 expression when dietary K+ was increased. K+ supplementation also demonstrated that Kcnj13+/- rats excreted more K+ on normal salt. The development of hypertension was not different when rats were challenged with high salt for 3 wk, although Kcnj13+/- rats excrete less Na+. Interestingly, chronic infusion of ML418 significantly increased Na+ and Cl- excretion after 14 days of high salt but did not alter salt-induced hypertension development. Here, we found that reduction of Kir7.1 function, either through genetic ablation or pharmacological inhibition, can influence renal electrolyte excretion but not to a sufficient degree to impact the development of SS hypertension.NEW & NOTEWORTHY To investigate the role of the Kir7.1 channel in salt-sensitive hypertension, its function was examined using complementary genetic and pharmacological approaches. The results revealed that although reducing Kir7.1 expression had some impact on maintaining K+ and Na+ balance, it did not lead to a significant change in the development or magnitude of salt-induced hypertension. Hence, it is probable that Kir7.1 works in conjunction with other basolateral K+ channels to fine-tune membrane potential.

Abnormal cardiac metabolism is a key factor in the development of cardiovascular diseases. Consequently, there has been considerable emphasis on researching and developing drugs that regulate metabolism. This study employed bibliometric methods to comprehensively and objectively analyze the relevant literature, offering insights into the knowledge dynamics in this field. The data source for this study was the Web of Science Core Collection (WoSCC), from which the collected data were imported into bibliometric software for analysis. The United States was the leading contributor, accounting for 38.33&#xa0;% of publications. The University of Washington and Damian J. Tyler were the most active institution and author, respectively. The American Journal of Physiology-Heart and Circulatory Physiology, Journal of Molecular and Cellular Cardiology, Cardiovascular Research, Circulation Research, and American Journal of Physiology-Endocrinology and Metabolism were highly influential journals that published numerous high-quality articles on cardiac metabolism. Common keywords in this research area included heart failure, insulin resistance, skeletal muscle, mitochondria, as well as topic words such as cardiac metabolism, fatty acid oxidation, glucose metabolism, and myocardial metabolism. Co-citation analysis has shown that research on heart failure and in vitro modeling of cardiovascular disease has gained prominence in recent years and making it a research hotspot. Research on cardiac metabolism is steadily growing, with a specific focus on heart failure and the interplay between mitochondrial dysfunction, insulin resistance, and cardiac metabolism. An emerging trend in this field involves the enhancement of maturation in human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM) through the manipulation of cardiac metabolism.

We have previously observed that prolonged administration of rapamycin, an inhibitor targeting the mammalian target of rapamycin complex (mTORC)1, partially reduced hypertension and alleviated kidney inflammation in Dahl salt-sensitive (SS) rats. In contrast, treatment with PP242, an inhibitor affecting both mTORC1/mTORC2, not only completely prevented hypertension but also provided substantial protection against kidney injury. Notably, PP242 exhibited potent natriuretic effects that were not evident with rapamycin. The primary objective of this study was to pinpoint the specific tubular sites responsible for the natriuretic effect of PP242 in SS rats subjected to either 0.4% NaCl (normal salt) or 4.0% NaCl (high salt) diet. Acute effects of PP242 on natriuretic, diuretic, and kaliuretic responses were determined in unanesthetized SS rats utilizing benzamil, furosemide, or hydrochlorothiazide [inhibitors of epithelial Na+ channel (ENaC), Na-K-2Cl cotransporter (NKCC2), or Na-Cl cotransporter (NCC), respectively] either administered alone or in combination. The findings indicate that the natriuretic effects of PP242 in SS rats stem predominantly from the inhibition of NCC and a reduction of ENaC open probability. Molecular analysis revealed that mTORC2 regulates NCC activity through protein phosphorylation and ENaC activity through proteolytic cleavage in vivo. Evidence also indicated that PP242 also prevents the loss of K+ associated with the inhibition of NCC. These findings suggest that PP242 may represent an improved therapeutic approach for antihypertensive intervention, potentially controlling blood pressure and mitigating kidney injury in salt-sensitive human subjects.NEW & NOTEWORTHY This study explored mechanisms underlying the natriuretic effects of mammalian target of rapamycin protein complex 2 inhibition using PP242 and revealed both epithelial Na+ channel and Na-Cl cotransporter in the distal tubular segments were potentially inhibited. These observations, with prior lab evidence, indicate that PP242 prevents hypertension via its potent inhibitory effects on these specific sodium transporters and by reducing renal immune responses. This dual action, coupled with potassium sparing effects, suggests an improved approach for managing hypertension and associated kidney damage.

Renal microcirculation plays a pivotal role in kidney function by maintaining structural and functional integrity, facilitating oxygen and nutrient delivery, and waste removal. However, a thorough bibliometric analysis in this area remains lacking. Therefore, we aim to provide valuable insights through a bibliometric analysis of renal microcirculation literature using the Web of Science database. We collected renal microcirculation-related publications from the Web of Science database from January 01, 1990, to December 31, 2022. The co-authorship of authors, organizations, and countries/regions was analyzed with VOSviewer1.6.18. The co-occurrence of keywords and co-cited references were analyzed using CiteSpace6.1.R6 software to generate visualization maps. Additionally, burst detection was applied to keywords and cited references to forecast research hotspots and future trends. Our search yielded 7462 publications, with the American Journal of Physiology-Renal Physiology contributing the most articles. The United States, Mayo Clinic, and Lerman Lilach O emerged with the highest publication count, indicating their active collaborations. 'Type 2 diabetes' was the most significant keyword cluster, and 'diabetic kidney disease' was the largest cluster of cited references. 'Cardiovascular outcome' and 'diabetic kidney diseases' were identified as keywords in their burst period over the past three years. Our bibliometric analysis illuminates the contours of nephrology and microcirculation research, revealing a landscape ripe for challenges and the seeds of future scientific innovation. While the trends discerned from the literature emerging opportunities in diagnostic innovation, renal microcirculation research, and precision medicine interventions, their translation to clinical practice is anticipated to be a deliberate process.

Whole-brain irradiation (WBI, also known as whole-brain radiation therapy) is a mainstay treatment modality for patients with multiple brain metastases. It is also used as a prophylactic treatment for microscopic tumors that cannot be detected by magnetic resonance imaging. WBI induces a progressive cognitive decline in&#x2009;~&#x2009;50% of the patients surviving over 6&#xa0;months, significantly compromising the quality of life. There is increasing preclinical evidence that radiation-induced injury to the cerebral microvasculature and accelerated neurovascular senescence plays a central role in this side effect of WBI. To better understand this side effect, male C57BL/6 mice were first subjected to a clinically relevant protocol of fractionated WBI (5&#xa0;Gy, two doses per week, for 4&#xa0;weeks). Nine months post the WBI treatment, we applied two-photon microscopy and Doppler optical coherence tomography to measure capillary red-blood-cell (RBC) flux, capillary morphology, and microvascular oxygen partial pressure (PO2) in the cerebral somatosensory cortex in the awake, head-restrained, WPI-treated mice and their age-matched controls, through a cover-glass-sealed chronic cranial window. Thanks to the extended penetration depth with the fluorophore - Alexa680, measurements of capillary blood flow properties (e.g., RBC flux, speed, and linear density) in the cerebral subcortical white matter were enabled. We found that the WBI-treated mice exhibited a significantly decreased capillary RBC flux in the white matter. WBI also caused a significant reduction in capillary diameter, as well as a large (although insignificant) reduction in segment density at the deeper cortical layers (e.g., 600-700&#xa0;&#x3bc;m), while the other morphological properties (e.g., segment length and tortuosity) were not obviously affected. In addition, we found that PO2 measured in the arterioles and venules, as well as the calculated oxygen saturation and oxygen extraction fraction, were not obviously affected by WBI. Lastly, WBI was associated with a significant increase in the erythrocyte-associated transients of PO2, while the changes of other cerebral capillary PO2 properties (e.g., capillary mean-PO2, RBC-PO2, and InterRBC-PO2) were not significant. Collectively, our findings support the notion that WBI results in persistent cerebral white matter microvascular impairment, which likely contributes to the WBI-induced brain injury and cognitive decline. Further studies are warranted to assess the WBI-induced changes in brain tissue oxygenation and malfunction of the white matter microvasculature as well.

Fate mapping and genetic manipulation of renin cells have relied on either noninducible Cre lines that can introduce the developmental effects of gene deletion or bacterial artificial chromosome transgene-based inducible models that may be prone to spurious and/or ectopic gene expression. To circumvent these problems, we generated an inducible mouse model in which CreERT2 is under the control of the endogenous Akr1b7 gene, an independent marker of renin cells that is expressed in a few extrarenal tissues. We confirmed the proper expression of Cre using Akr1b7CreERT2/+;R26RmTmG/+ mice in which Akr1b7+/renin+ cells become green fluorescent protein (GFP)+ upon tamoxifen administration. In embryos and neonates, GFP was found in juxtaglomerular cells, along the arterioles, and in the mesangium, and in adults, GFP was present mainly in juxtaglomerular cells. In mice treated with captopril and a low-salt diet to induce recruitment of renin cells, GFP extended along the afferent arterioles and in the mesangium. We generated Akr1b7CreERT2/+;Ren1cFl/-;R26RmTmG/+ mice to conditionally delete renin in adult mice and found a marked reduction in kidney renin mRNA and protein and mean arterial pressure in mutant animals. When subjected to a homeostatic threat, mutant mice were unable to recruit renin+ cells. Most importantly, these mice developed concentric vascular hypertrophy ruling out potential developmental effects on the vasculature due to the lack of renin. We conclude that Akr1b7CreERT2 mice constitute an excellent model for the fate mapping of renin cells and for the spatial and temporal control of gene expression in renin cells.NEW & NOTEWORTHY Fate mapping and genetic manipulation are important tools to study the identity of renin cells. Here, we report on a novel Cre mouse model, Akr1b7CreERT2, for the spatial and temporal regulation of gene expression in renin cells. Cre is properly expressed in renin cells during development and in the adult under basal conditions and under physiological stress. Moreover, renin can be efficiently deleted in the adult, leading to the development of concentric vascular hypertrophy.

Chronic obstructive pulmonary disease (COPD) has become a major global healthcare issue due to its high prevalence and mortality rates. Increasing evidence suggests that autophagy plays a role in the development of COPD, yet there is a lack of bibliometric analyses on literature related to autophagy and COPD. Therefore, this study aims to summarize the current research status, research direction, and research hotspots in the literature related to COPD and autophagy. A search was conducted on the Web of Science Core Collection for literature related to COPD and autophagy from October 2004 to October 2024. Subsequently, bibliometric and visualization analyses were performed on the included publications using R software, CiteSpace, and VOSviewer. A total of 481 published articles across 229 journals related to COPD and autophagy were included. During the study period, there was a trend of continuous growth in both the annual number of publications and citations in this field. The United States had the highest centrality, while China was the most productive country. Major research institutions included Maastricht University, Harvard University, and Jikei University. The American Journal of Physiology-Lung Cellular and Molecular Physiology, International Journal of Chronic Obstructive Pulmonary Disease, and Autophagy are the most influential journals in this field. The author with the most published papers is Araya J, while Choi AMK is the most influential author. Frequently appearing keywords include "oxidative stress," "obstructive pulmonary disease," "aging," "apoptosis," and "mitophagy." This bibliometric study helps researchers quickly understand the research overview of autophagy and COPD, thus providing new insights and directions for future research in this field.

Alveolar regeneration represents a critical research direction in respiratory disease treatment. Despite the surge in studies following the COVID-19 pandemic, comprehensive bibliometric analysis to systematically evaluate global research trends and future directions remains lacking. This study employed bibliometric methodology to analyze 1564 publications related to alveolar regeneration from 1974 to 2024 using the Web of Science Core Collection database. Data visualization and analysis were conducted using VOSviewer (version 1.6.19), CiteSpace (version 6.2.R3), and the biblioshiny R package. The analysis encompassed 68 countries, 1930 institutions, and 9150 researchers across 658 journals. The United States leads with 601 publications and 32,172 citations, with Harvard University as the most influential institution. The American Journal of Respiratory and Critical Care Medicine has the highest impact factor (19.3), while the American Journal of Physiology-Lung Cellular and Molecular Physiology has the most co-citations (2,402). Edward E. Morrisey is the most prolific author, and C. E. Barkauskas has the highest co-citations. Keyword analysis revealed six major research clusters: stem cells and regenerative medicine, acute lung injury and fibrosis, COVID-19-related research, chronic lung disease repair, cellular behavior and molecular mechanisms, and post-pneumonectomy regeneration. Thematic mapping indicates future research should prioritize lung injury repair mechanisms, matrix environment in tissue regeneration, stem cell therapeutics, and immune regulation in lung injury repair. This first comprehensive 50-year bibliometric analysis of alveolar regeneration reveals the evolutionary trend from basic mechanistic exploration toward clinical translational applications, providing important reference for researchers and funding agencies.

Heart failure is one of the major public health problems in the world. In recent years, more and more attention has been paid to the relationship between heart failure and mitochondrial function. In the past 2 decades, a growing number of research papers in this field have been published. This study conducted a bibliometric analysis of the published literature on the relationship between MF and HF in the past 20&#xa0;years by utilizing Microsoft Excel 2019, Biblio metric analysis platform, WoSCC database, VosViewer and Citespace. The results show that the papers have increased year by year and China and the United States are the leading countries in this field, as well as the countries with the most cooperation and exchanges. University of california system is the research institution with the greatest impacts on research results, and Yip H.K. is the author with more papers. The American Journal of Physiology-heart and Circulatory Physiology is probably the most popular magazine. At present, most of the published articles on mitochondria and HF are cited from internationally influential journals. The research focus includes oxidative stress, metabolic dysfunction, mitochondrial Ca2+ homeostasis imbalance, mitochondrial quality control and mitochondrial dysfunction mediated by inflammation in the pathogenesis of HF. Targeted regulating of mitochondria will be the keynote of future research on prevention and treatment of HF.

Long COVID affects approximately 5&#xa0;million people in Africa. This disease is characterized by persistent symptoms or new onset of symptoms after an acute SARS-CoV-2 infection. Specifically, the most common symptoms include a range of cardiovascular problems such as chest pain, orthostatic intolerance, tachycardia, syncope, and uncontrolled hypertension. Importantly, these conditions appear to have endothelial dysfunction as the common denominator, which is often due to impaired nitric oxide (NO) mechanisms. This review discusses the role of mechanisms contributing to endothelial dysfunction in Long COVID, particularly in people living with HIV. Recent studies have reported that increased inflammation and oxidative stress, frequently observed in Long COVID, may contribute to NO dysfunction, ultimately leading to decreased vascular reactivity. These mechanisms have also been reported in people living with HIV. In regions like Africa, where HIV infection is still a major public health challenge with a prevalence of approximately 26&#xa0;million people in 2022. Specifically, endothelial dysfunction has been reported as a major mechanism that appears to contribute to cardiovascular diseases and the intersection with Long COVID mechanisms is of particular concern. Further, it is well established that this population is more likely to develop Long COVID following infection with SARS-CoV-2. Therefore, concomitant infection with SARS-CoV-2 may lead to accelerated cardiovascular disease. We outline the details of the worsening health problems caused by Long COVID, which exacerbate pre-existing conditions such as endothelial dysfunction. The overlapping mechanisms of HIV and SARS-CoV-2, particularly the prolonged inflammatory response and chronic hypoxia, may increase susceptibility to Long COVID. Addressing these overlapping health issues is critical as it provides clinical entry points for interventions that could improve and enhance outcomes and quality of life for those affected by both HIV and Long COVID in the region.

Activation of G protein-coupled estrogen receptor 1 (GPER1) elicits antihypertensive actions in different animal models. The endothelin-1 signaling system plays a fundamental role in blood pressure regulation. Lack of functional endothelin receptor B (ETB) evokes hypertension and salt sensitivity. GPER1 and ETB interact to promote urinary sodium excretion in female rats. We hypothesized that activation of GPER1 protects against hypertension and salt sensitivity induced by ETB antagonism in female rats. Female Sprague-Dawley rats were implanted with radiotelemetry. Animals were then subjected to ovariectomy and simultaneously implanted with minipumps to deliver either the GPER1 agonist G1 or its corresponding vehicle. Two weeks post surgery, we initiated treatment of rats with the ETB antagonist A-192621. Animals were maintained on a normal-salt diet and then challenged with a high-salt diet for an additional 5 days. Assessment of mean arterial blood pressure revealed an increase in vehicle-treated, but not G1-treated, rats in response to ovariectomy. A-192621 increased blood pressure in normal-salt diet-fed vehicle- and G1-treated rats. G1 improved the circadian blood pressure rhythms that were disrupted in A-192621-treated ovariectomized rats. Thus, although systemic GPER1 activation did not protect ovariectomized rats from hypertension and salt sensitivity induced by ETB antagonism, it maintained circadian blood pressure rhythms. Functional ETB is required to elicit the antihypertensive actions of GPER1. Additional studies are needed to improve our understanding of the interaction between G protein-coupled receptors in regulating circadian blood pressure rhythm.NEW & NOTEWORTHY Systemic G protein-coupled estrogen receptor 1 (GPER1) activation in rats prevents the increase in blood pressure evoked by ovariectomy. Blockade of endothelin receptor B negates the blood pressure-lowering impact of GPER1 in ovariectomized rats. Endothelin receptor B plays an important role in mediating the blood pressure-lowering action of GPER1 activation in female rats.

Whole brain irradiation (WBI), a commonly employed therapy for multiple brain metastases and as a prophylactic measure after cerebral metastasis resection, is associated with a progressive decline in neurocognitive function, significantly impacting the quality of life for approximately half of the surviving patients. Recent preclinical investigations have shed light on the multifaceted cerebrovascular injury mechanisms underlying this side effect of WBI. In this study, we aimed to test the hypothesis that WBI induces endothelial senescence, contributing to chronic disruption of the blood-brain barrier (BBB) and microvascular rarefaction. To accomplish this, we utilized transgenic p16-3MR mice, which enable the identification and selective elimination of senescent cells. These mice were subjected to a clinically relevant fractionated WBI protocol (5 Gy twice weekly for 4 weeks), and cranial windows were applied to both WBI-treated and control mice. Quantitative assessment of BBB permeability and capillary density was performed using two-photon microscopy at the 6-month post-irradiation time point. The presence of senescent microvascular endothelial cells was assessed by imaging flow cytometry, immunolabeling, and single-cell RNA-sequencing (scRNA-seq). WBI induced endothelial senescence, which associated with chronic BBB disruption and a trend for decreased microvascular density in the mouse cortex. In order to investigate the cause-and-effect relationship between WBI-induced senescence and microvascular injury, senescent cells were selectively removed from animals subjected to WBI treatment using Navitoclax/ABT263, a well-known senolytic drug. This intervention was carried out at the 3-month post-WBI time point. In WBI-treated mice, Navitoclax/ABT263 effectively eliminated senescent endothelial cells, which was associated with decreased BBB permeability and a trend for increased cortical capillarization. Our findings provide additional preclinical evidence that senolytic treatment approaches may be developed for prevention of the side effects of WBI.