American journal of physiology. Heart and circulatory physiology最新文献

{"title":"Acceleration of age-related impairments in vascular function in women: interrogation of the (un)usual hormonal suspects.","authors":"Kylee S West, Nathaniel D M Jenkins","doi":"10.1152/ajpheart.00730.2024","DOIUrl":"10.1152/ajpheart.00730.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1387-H1389"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in the functional morphology of coronary arteries in embryonic mice.","authors":"Shion Nagasawa, Masami Kodama, Ryu Hagiwara, Kazuho Sakamoto, Koichi Nishiyama, Yuichiro Arima, Hiroki Kurihara, Junko Kurokawa","doi":"10.1152/ajpheart.00186.2024","DOIUrl":"10.1152/ajpheart.00186.2024","url":null,"abstract":"<p><p>Sex differences in the development and progression of cardiovascular disease manifest across multiple life stages. These differences are associated with variations in cardiovascular morphology and function between the sexes. Although estrogens and sex hormones are associated with sex differences in cardiovascular diseases in reproductive adults, the molecular mechanisms of cardiovascular sex differences during development are largely unknown. Thus, we investigated sex differences in cardiovascular development. We used a newly developed coronary arteriogram system to visualize the morphology of the coronary arteries in murine anterior surface ventricles at embryonic day 17.5 by injecting nanoparticle ink at a constant pressure. No sex difference was found in the length of ventricle. Based on the boundary value of the distribution of that length, the hearts were divided into \"long\" and \"short\" groups and the diameters of the left coronary arteries were analyzed. The mean diameter of the coronary arteries was significantly smaller in females than in males only in the group with the longer length of ventricle. This ventricular size-specific sex difference was observed in the presence of vasodilators such as NOC7 (1-Hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene). When NOC7 was perfused into the left coronary arteries of embryonic day 17.5 mice, females with longer ventricles showed larger left coronary arteries than males. These sex differences in vasodilation capacity suggest that factors related to drug reactivity such as signaling pathways are present at a late embryonic stage. These results indicate that sex differences in the functional morphology of the left coronary arteries exist at a late embryonic stage in mice.<b>NEW & NOTEWORTHY</b> This study introduces a novel coronary angiography method for analyzing murine embryonic hearts, revealing sex differences in coronary artery morphology and contractile function in the late stage of the fetal period. By categorizing heart components based on size, we unveil nuanced insights into sexual dimorphism during this critical fetal period. This work contributes insights into the early origins of sexual dimorphism in coronary vessels, laying the foundation for further understanding of cardiovascular development.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1390-H1399"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A zebrafish model to study <i>RRAGD</i> variants associated cardiomyopathy.","authors":"Irene Sambri, Francesco Trepiccione","doi":"10.1152/ajpheart.00695.2024","DOIUrl":"10.1152/ajpheart.00695.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1343-H1344"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Creating diversity, equity, inclusion, and accessibility statements for your CV: a resource guide to effectiveness and comprehensiveness.","authors":"Jesse D Moreira-Bouchard, Jason Cunha, Brian S Tao, Hahnbie Kim, Joshua Lepson, Evan J Nessen, Zachary J Milstone, Nathaniel Fisher, Nancy Clinton, Lisa M Roberts, Maria A Serrano, Deepa M Gopal, Emelia J Benjamin, Kaku So-Armah, Jessica L Fetterman","doi":"10.1152/ajpheart.00610.2024","DOIUrl":"10.1152/ajpheart.00610.2024","url":null,"abstract":"<p><p>Diversity in academic medicine and research enhances the quality of the science produced and the efficacy of patient care. Diversity, equity, inclusion, and accessibility (DEIA) statements have recently been suggested or required by academic job postings as a way to measure candidate's commitments to fostering DEIA in their role. In this perspective, we discuss steps to craft effective DEIA statements that convey your actions in, and commitment to, DEIA. We recognize that mandating DEIA statements may actually result in inauthentic or disingenuous statements and offer solutions to encouraging academics to arrive at a meaningful statement that represents their own perspectives on diversity. Last, we provide examples of DEIA statements from three academics at different career points.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1376-H1383"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.","authors":"Gaurav Sharma, Shyam S Chaurasia, Mark A Carlson, Paras K Mishra","doi":"10.1152/ajpheart.00539.2024","DOIUrl":"10.1152/ajpheart.00539.2024","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is characterized by chronic hyperglycemia, and despite intensive glycemic control, the risk of heart failure in patients with diabetes remains high. Diabetes-induced heart failure (DHF) presents a unique metabolic challenge, driven by significant alterations in cardiac substrate metabolism, including increased reliance on fatty acid oxidation, reduced glucose utilization, and impaired mitochondrial function. These metabolic alterations lead to oxidative stress, lipotoxicity, and energy deficits, contributing to the progression of heart failure. Emerging research has identified novel mechanisms involved in the metabolic remodeling of diabetic hearts, such as autophagy dysregulation, epigenetic modifications, polyamine regulation, and branched-chain amino acid (BCAA) metabolism. These processes exacerbate mitochondrial dysfunction and metabolic inflexibility, further impairing cardiac function. Therapeutic interventions targeting these pathways-such as enhancing glucose oxidation, modulating fatty acid metabolism, and optimizing ketone body utilization-show promise in restoring metabolic homeostasis and improving cardiac outcomes. This review explores the key molecular mechanisms driving metabolic remodeling in diabetic hearts, highlights advanced methodologies, and presents the latest therapeutic strategies for mitigating the progression of DHF. Understanding these emerging pathways offers new opportunities to develop targeted therapies that address the root metabolic causes of heart failure in diabetes.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1327-H1342"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thy and mighty: the importance of T3 thyroid hormone on dyadic structure and function in cardiac health and disease.","authors":"Charlotte E R Smith","doi":"10.1152/ajpheart.00735.2024","DOIUrl":"10.1152/ajpheart.00735.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1384-H1386"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolites and metabolism in vascular calcification: links between adenosine signaling and the methionine cycle.","authors":"Parya Behzadi, Cynthia St Hilaire","doi":"10.1152/ajpheart.00267.2024","DOIUrl":"10.1152/ajpheart.00267.2024","url":null,"abstract":"<p><p>The global population of individuals with cardiovascular disease is expanding, and a key risk factor for major adverse cardiovascular events is vascular calcification. The pathogenesis of cardiovascular calcification is complex and multifaceted, with external cues driving epigenetic, transcriptional, and metabolic changes that promote vascular calcification. This review provides an overview of some of the lesser understood molecular processes involved in vascular calcification and discusses the links between calcification pathogenesis and aspects of adenosine signaling and the methionine pathway; the latter of which salvages the essential amino acid methionine, but also provides the substrate critical for methylation, a modification that regulates the function and activity of DNA and proteins. We explore the complex and dynamic nature of osteogenic reprogramming underlying intimal atherosclerotic calcification and medial arterial calcification (MAC). Atherosclerotic calcification is more widely studied; however, emerging studies now show that MAC is a significant pathology independent from atherosclerosis. Furthermore, we emphasize metabolite and metabolic-modulating factors that influence vascular calcification pathogenesis. Although the contributions of these mechanisms are more well-define in relation to atherosclerotic intimal calcification, understanding these pathways may provide crucial mechanistic insights into MAC and inform future therapeutic approaches. Herein, we highlight the significance of adenosine and methyltransferase pathways as key regulators of vascular calcification pathogenesis.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1361-H1375"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of T cells in vascular aging, hypertension, and atherosclerosis.","authors":"Theodore M DeConne, David J Buckley, Daniel W Trott, Christopher R Martens","doi":"10.1152/ajpheart.00570.2024","DOIUrl":"10.1152/ajpheart.00570.2024","url":null,"abstract":"<p><p>Vascular dysfunction has emerged as a significant risk factor for the development of cardio- and cerebrovascular diseases (CVDs), which are currently the leading cause of morbidity and mortality worldwide. T lymphocytes (T cells) have been shown to be important modulators of vascular function in primary aging and CVDs, likely by producing inflammatory cytokines and reactive oxygen species that influence vasoprotective molecules. This review summarizes the role of T cells on vascular function in aging, hypertension, and atherosclerosis in animals and humans, and discusses potential T-cell targeted therapeutics to prevent, delay, or reverse vascular dysfunction.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1345-H1360"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perinatal iron deficiency alters the cardiac proteome and mitochondrial function in neonatal offspring.","authors":"Claudia D Holody, Andrew G Woodman, Chunpeng Nie, Si Ning Liu, Daniel Young, Alyssa Wiedemeyer, Rowan Carpenter, Ronan M N Noble, Daniel Graf, Antoine Dufour, Helene Lemieux, Stephane L Bourque","doi":"10.1152/ajpheart.00412.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00412.2024","url":null,"abstract":"<p><p><i>Aims:</i> Iron deficiency (ID) is common during gestation and early infancy and can alter developmental trajectories with lasting consequences on cardiovascular health. Iron plays a critical role in systemic oxygen transport (via hemoglobin) and aerobic respiration (as a component of mitochondrial complexes). Perinatal ID has been shown to cause cardiac dysfunction in neonates, but the mechanisms underlying these changes have not been characterized. Here, we examined the effects of perinatal ID on cardiac mitochondrial function in the early postnatal period in rats. <i>Methods and Results:</i> Female rats were fed an iron-restricted or iron-replete diet before and during pregnancy. Offspring hearts were collected postmortem for quantitative shotgun proteomic analysis (postnatal days [PD]0 and 28) and mitochondrial function was assessed by high-resolution respirometry (at PD0, 14 and 28). Markers of oxidative stress were measured by fluorescence microscopy and assessment of antioxidant gene expression profiles. Both male and female ID pups had reduced body weight and increased relative heart weights at all time points assessed, despite recovering from anemia by PD28. Proteomics analysis revealed dysregulation of mitochondrial proteins by ID, and these differences were most pronounced in males. In male hearts, ID increased mitochondrial content and decreased normalized mitochondrial respiration through the NADH-pathway, succinate-pathway, and FAO-pathway. <i>Conclusions:</i> ID causes changes in cardiac mitochondrial function in neonates, which may reflect an inadequate or maladaptive compensation during the transition from intrauterine to extrauterine life. Further, the results presented herein, which were stratified by offspring sex, underscore the need for follow-up studies to directly assess differences in the way male and female offspring cope with ID as a perinatal stressor.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sub-component analysis of the directional sensitivity of dynamic cerebral autoregulation.","authors":"Ronney B Panerai, Aaron Davies, Abdulaziz Alshehri, Lucy C Beishon, Jatinder S Minhas","doi":"10.1152/ajpheart.00498.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00498.2024","url":null,"abstract":"<p><p>The origin of the directional sensitivity (DS) of dynamic cerebral autoregulation (dCA) is not known. In 140 healthy participants (67 male, 27.5 ± 6.1 years old), middle cerebral artery velocity (MCAv, transcranial Doppler), arterial blood pressure (ABP, Finometer), and end-tidal CO2 (EtCO₂, capnography) were recorded at rest. Critical closing pressure (CrCP) and resistance-area product (RAP) were obtained for each cardiac cycle, as well as mean MCAv and ABP (MAP). The integrated positive and negative derivatives of MAP (MAP_‫D, MAP_-D) were used as simultaneous inputs to an autoregressive moving average model to generate two distinct MCAv step responses. Similar models allowed estimation of corresponding MAP-CrCP and MAP-RAP responses to step changes in MAP_‫D and MAP_-D. The strength of directional sensitivity (ΔDS) was expressed by the difference in mean values of the step responses for the time interval 12-18 s. ΔDS was significant for MCAv (8.5 ± 46.9% vs 26.7 ± 42.0%, p<0.001) and RAP (-93.9 ± 48.1 vs -74.5 ± 43.0%, p<0.001), respectively for MAP_‫D and MAP_-D inputs, but not for CrCP (2.2 ± 48.1% vs 0.72 ± 42.9%, p=0.76). Compared to males, female participants had higher MCAv (63.9 ± 15.6 cm/s vs 55.4 ± 12.9 cm/s, p<0.001), but lower EtCO₂ (p<0.001) and RAP (p=0.015). Sex did not influence ΔDS for any of the three step responses. The presence of directional sensitivity in the RAP, but not in the CrCP transfer function, suggests the origin could be solely myogenic, without metabolic involvement.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}