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

{"title":"Hypertrophic heart failure promotes gut dysbiosis and gut leakage in interleukin 10-deficient mice.","authors":"Prabhat Ranjan, Sumanta Kumar Goswami, Roshan Kumar Dutta, Karen Colin, Harish Chandra Pal, Qinkun Zhang, Hind Lal, Ram Prasad, Suresh Kumar Verma","doi":"10.1152/ajpheart.00323.2024","DOIUrl":"10.1152/ajpheart.00323.2024","url":null,"abstract":"<p><p>Heart failure (HF) is a leading cause of death worldwide. We have shown that pressure overload (PO)-induced inflammatory cell recruitment leads to heart failure in IL-10 knockout (KO) mice. However, it is unclear whether PO-induced inflammatory cells also target the gut mucosa, causing gut dysbiosis and leakage. We hypothesized that transverse aortic constriction (TAC) exacerbates immune cell homing to the gut (small intestine and colon), promoting dysbiosis and gut leakage in IL-10 KO mice. HF was induced in 8- to 10-wk-old C57BL/6J wild-type (WT) and B6.129P2-Il10tm1Cgn/J mutant (IL-10 KO) male and female mice by TAC and cardiac function was measured using visual sonics VEVO 3100. Fourteen days post-TAC, levels of monocytes, macrophages, neutrophils, and proinflammatory cytokines were measured in blood and gut. Gut dysbiosis was assessed via 16S rRNA sequencing in feces at 56 days post-TAC. IL-10 KO mice showed worsened cardiac dysfunction post-TAC. TAC worsened monocytes, and neutrophils infiltration in systemic circulation and facilitated their homing to the gut in IL-10 KO mice. Intriguingly, proinflammatory cytokines level was increased in blood, and gut of IL-10 KO mice following TAC. Furthermore, IL-10 expression was reduced in the colon of WT mice post-TAC. Moreover, TAC exacerbated gut dysbiosis in IL-10 KO mice. Finally, an impaired intestinal permeability was noted in IL-10 KO mice post-TAC. In conclusion, TAC-induced systemic inflammation leads to gut dysbiosis and impaired gut permeability in IL-10 KO mice, indicating IL-10's potential role in regulating intestinal integrity and microbiota balance during heart failure.<b>NEW & NOTEWORTHY</b> IL-10, crucial for systemic inflammation regulation and gut mucosal homeostasis, was investigated using IL-10 knockout (KO) mice. Exacerbated gut inflammation was observed post-transverse aortic constriction (TAC) in IL-10-depleted mice, whereas wild-type (WT) mice showed reduced IL-10 gene expression in colon and ileum. TAC induced gut dysbiosis and leakage in IL-10 KO mice, suggesting a link between enhanced inflammatory signaling in heart failure and multi-organ damage via gut dysbiosis and leakage.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H447-H459"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031840","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":"Favorable alterations in ventricular-arterial interactions across the menstrual cycle in healthy premenopausal women.","authors":"Ninette Shenouda, Joseph M Stock, Nicholas V Chouramanis, Zoe R Lincoln, Megan M Wenner, Julio A Chirinos, David G Edwards","doi":"10.1152/ajpheart.00363.2024","DOIUrl":"10.1152/ajpheart.00363.2024","url":null,"abstract":"<p><p>Increased arterial wave reflections can increase left ventricular wasted pressure effort (WPE) and cardiovascular disease risk. Naturally menstruating women experience fluctuations in sex hormones with known cardioprotective effects. We sought to determine whether hormonal fluctuations alter arterial hemodynamics or wave reflections, and thereby WPE, or contribute to sex differences. We hypothesized that premenopausal women would have favorable wave reflection changes and reduced WPE during high- versus low-hormone cycle phases and compared with men. We tested 13 women (28 ± 7 yr) during the early follicular (EF, <i>cycle days 3</i> ± <i>1</i>), late follicular (LF, <i>cycle days 12</i> ± <i>2</i>), and mid-luteal (ML, <i>cycle days 22</i> ± <i>3</i>) phases. Eleven men (28 ± 3 yr) underwent time-matched visits. Sex hormones and arterial hemodynamics were measured at all visits. Wave reflection indices and WPE were assessed via aortic pressure-flow analyses. We observed sex-by-visit interactions for WPE and total peripheral resistance (TPR; both <i>P</i> < 0.01). Women showed favorable reductions in WPE (EF: 2,758 ± 966 and LF: 2,489 ± 1,230 vs. ML: 1,954 ± 1,085 mmHg·ms, both <i>P</i> < 0.05) and TPR (EF: 1,885 ± 271 vs. ML: 1,699 ± 255 dyn·s·cm^-5, <i>P</i> = 0.01) from low- to high-hormone phases. These reductions were not observed in men and were not paralleled in classic wave reflection indices (<i>P</i> > 0.05). Increased estradiol predicted a reduction in TPR (<i>R</i>² = 0.45, <i>P</i> < 0.001), whereas TPR, reflected wave amplitude, and timing of wave reflection predicted reductions in WPE (<i>R</i>² = 0.71, <i>P</i> < 0.001). These data implicate a role of estradiol on the peripheral vasculature, leading to reduced left ventricular WPE, suggesting a need to consider cycle phases when assessing ventricular load in naturally menstruating women.<b>NEW & NOTEWORTHY</b> Using aortic pressure-flow analyses, we demonstrate favorable reductions in left ventricular wasted pressure effort across menstrual cycle phases in healthy premenopausal women, but not across time-matched visits in men. Increases in estradiol were related to changes in total peripheral resistance, which, along with reflected wave amplitude and timing, leads to a reduced wasted pressure effort. Our findings suggest a need to consider sex hormones and cycle phases when assessing ventricular load in naturally menstruating women.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H648-H657"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381524","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":"Cardiac acetylcholinesterase and butyrylcholinesterase have distinct localization and function.","authors":"Dominika Dingová, Matej Kučera, Tibor Hodbod, Rodolphe Fischmeister, Eric Krejci, Anna Hrabovská","doi":"10.1152/ajpheart.00672.2024","DOIUrl":"10.1152/ajpheart.00672.2024","url":null,"abstract":"<p><p>Cholinesterase (ChE) inhibitors are under consideration for use in the treatment of cardiovascular pathologies. A prerequisite to advancing ChE inhibitors into the clinic is their thorough characterization in the heart. The aim here was to provide a detailed analysis of cardiac ChE to understand their molecular composition, localization, and physiological functions. A battery of biochemical, microscopic, and physiological experiments was used to analyze two known ChE, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), in hearts of mutant mice lacking different ChE molecular forms. Overall, AChE activity was exceeded by BChE, while it was localized mainly in the atria and the ventricular epicardium of the heart base. AChE was anchored by collagen Q (ColQ) in the basal lamina or by PRiMA at the plasma membrane and co-localized with the neuronal marker TUJ1. In the absence of anchored AChE, the heart rate was unresponsive to a ChE inhibitor. BChE, the major ChE in the heart, was detected predominantly in ventricles, presumably as a precursor (soluble monomers/dimers). Mice lacking BChE were more sensitive to a ChE inhibitor. Nevertheless, the overall impact on heart physiology was subtle, showing mainly a role in cholinergic antagonism to the positive inotropic effect of β-adrenergic stimulation. Our results help to unravel the mechanisms of ChE in cardiovascular pathologies and provide a foundation to facilitate the design of novel, more effective pharmacotherapies, which may reduce morbidity and mortality of patients with various heart diseases.<b>NEW & NOTEWORTHY</b> Inhibition of cholinesterases has therapeutic potential in cardiovascular pathologies. Both acetylcholinesterase and butyrylcholinesterase are present in the heart. Each cholinesterase has distinct localization patterns in the heart and functions in cardiac physiology. Selective inhibition of acetylcholinesterase or butyrylcholinesterase may be used to alter specific cardiac functions. Butyrylcholinesterase polymorphism may have an impact on the outcome of the cholinesterase inhibitor treatment.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H526-H542"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998690","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":"Sexual dimorphism in right ventricular adaptation to pressure overload involves differential angiogenic response.","authors":"Erica R Seelemann, Sheethal Panchakshari, Parabhjot Kaur Labana, Maxwell M Wolverton, Yupu Deng, Haya Abdelwahab, Chris Consmueller, Duncan J Stewart, Ketul R Chaudhary","doi":"10.1152/ajpheart.00549.2024","DOIUrl":"10.1152/ajpheart.00549.2024","url":null,"abstract":"<p><p>This study investigated the sexual dimorphism in right ventricle (RV) remodeling in right heart failure susceptible Fischer CDF rats using the pulmonary artery banding (PAB) model. Echocardiography and hemodynamic measurements were performed in adult male and female Fischer CDF rats at 1- or 2-wk post-PAB. RV systolic pressure and RV hypertrophy were significantly elevated in PAB rats compared with sham control at 1- and 2-wk post-PAB; however, no differences were observed between male and female rats. Increase in cardiomyocyte cross-sectional area and RV end-diastolic diameter was observed in male rats compared with female rats at 2-wk post-PAB. Conversely, higher fractional area change and cardiac index were observed in female rats compared with male rats at 2-wk post-PAB. To explore the mechanisms, a focused PCR array was performed and higher expression of angiogenic genes, including sphingosine kinase-1 (<i>Sphk1</i>), was observed in the RV of female rats compared with male rats. Consistent with the higher angiogenic gene expression, female rats had a higher RV vascular density at 2-wk post-PAB compared with male rats. Female RV endothelial cells (RVECs) had better angiogenic ability compared with male cells that was potentiated by estradiol. Furthermore, effect of estradiol on RVECs was inhibited by Sphk1 inhibitor (PF-543). Together, female Fischer CDF rats develop adaptive RV remodeling post-PAB compared with maladaptive remodeling in male rats. Moreover, the adaptive remodeling in female rats is associated with better RV angiogenic response that may result from better angiogenic ability of female RVECs and proangiogenic effects of estradiol through Sphk1.<b>NEW & NOTEWORTHY</b> Female patients with pulmonary hypertension have better right ventricular adaptation compared with male. These sex differences were modeled in right heart failure susceptible Fischer CDF rat using pulmonary artery banding model. Preservation of right ventricular function in female rats is linked to better right ventricular angiogenic response that involves higher intrinsic angiogenic ability of female right ventricular endothelial cells together with the proangiogenic effects of female sex hormone estradiol through sphingosine kinase-1.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H496-H508"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051364","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":"Emerging roles of noncoding RNAs in cardiovascular pathophysiology.","authors":"Malak Abbas, Amadou Gaye","doi":"10.1152/ajpheart.00681.2024","DOIUrl":"10.1152/ajpheart.00681.2024","url":null,"abstract":"<p><p>This review comprehensively examines the diverse roles of noncoding RNAs (ncRNAs) in the pathogenesis and treatment of cardiovascular disease (CVD), focusing on microRNA (miRNA), long noncoding RNA (lncRNA), piwi-interacting RNA (piRNA), small-interfering RNA (siRNA), circular RNA (circRNA), and vesicle-associated RNAs. These ncRNAs are integral regulators of key cellular processes, including gene expression, inflammation, and fibrosis, and they hold great potential as both diagnostic biomarkers and therapeutic targets. The review highlights novel insights into how these RNA species, particularly miRNAs, lncRNAs, and piRNAs, contribute to various CVDs such as hypertension, atherosclerosis, and myocardial infarction. In addition, it explores the emerging role of extracellular vesicles (EVs) in intercellular communication and their therapeutic potential in cardiovascular health. The review underscores the need for continued research into ncRNAs and RNA-based therapies, with a focus on advancing delivery systems and expanding personalized medicine approaches to improve cardiovascular outcomes.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H603-H621"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363512","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":"Exposure to prenatal hypoxia impairs the function and structure of the carotid arteries in the adult offspring.","authors":"Murilo E Graton, Amanda A de Oliveira, Aryan Neupane, Anita Quon, Raven Kirschenman, Floor Spaans, Sandra T Davidge","doi":"10.1152/ajpheart.00859.2024","DOIUrl":"10.1152/ajpheart.00859.2024","url":null,"abstract":"<p><p>Prenatal hypoxia, a common pregnancy complication, leads to cardiac and vascular dysfunction, thereby increasing the risk of cardiovascular disease in the adult offspring. Carotid arteries are responsible for the majority of the blood flow to the brain/head, and carotid artery dysfunction is associated with life-threatening cardiovascular events, such as stroke. However, whether prenatal hypoxia exposure impacts the function of the carotid arteries in the adult offspring is not known. We hypothesize that prenatal hypoxia impairs carotid artery function in the adult male and female offspring. Sprague Dawley rats were exposed to normoxia (21% O₂) or hypoxia (11% O₂) from gestational day 15 to 21 (term = 22 days; <i>n</i> = 9 or 10/group). Carotid arteries were isolated from the 4-mo-old male and female offspring. Vasoconstrictor and vasodilatory properties were assessed by wire myography, and biomechanical properties (myogenic tone, circumferential stress, and strain) were assessed by pressure myography. Collagen deposition (Masson's trichrome stain) and elastin density (Verhoeff stain) were measured in carotid artery cryosections. Prenatal hypoxia did not impact vasoconstriction or vasorelaxation responses in carotid arteries from both offspring. However, in males, prenatal hypoxia reduced carotid artery myogenic tone development and increased circumferential strain, which coincided with lower collagen deposition and higher elastin density. In females, prenatal hypoxia tended to lower carotid artery circumferential strain (i.e., increased stiffness), without differences in myogenic tone or collagen/elastin density. Altogether, these data show that exposure to prenatal hypoxia affects the carotid arteries of the adult offspring in a sex-specific manner, which may impact the blood flow regulation to the brain.<b>NEW & NOTEWORTHY</b> Little is known about the (long-lasting) impact of pregnancy complications on offspring carotid artery function. We showed that, in adult male offspring, prenatal hypoxia decreased carotid artery myogenic tone and stiffness and changed collagen and elastin densities, whereas in females, prenatal hypoxia increased stiffness. These findings contribute to understanding sex-specific differences of adult offspring exposed to a suboptimal in utero environment on the carotid arteries, an important/easily accessible vascular bed for patient disease evaluation.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H518-H525"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063097","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 aortic valve inflammation and remodeling in chronic severe aortic regurgitation.","authors":"Carolina Tiraplegui, Mattie Garaikoetxea, Alba Sádaba, Susana San Ildefonso-García, Miriam Goñi-Olóriz, Amaya Fernández-Celis, Ernesto Martín-Núñez, Virginia Álvarez, Rafael Sádaba, Vidhu Anand, Eva Jover, Adela Navarro, Natalia López-Andrés","doi":"10.1152/ajpheart.00645.2024","DOIUrl":"10.1152/ajpheart.00645.2024","url":null,"abstract":"<p><p>Aortic regurgitation (AR) is more prevalent in males, although cellular and molecular mechanisms underlying the sex differences in prevalence and pathophysiology are unknown. This study evaluates the impact of sex on aortic valve (AV) inflammation and remodeling and the cellular differences in valvular interstitial cells (VICs) and valvular endothelial cells (VECs) in patients with AR. A total of 144 patients (27.5% female) with severe chronic AR were included. AVs were analyzed by imaging, histological, and molecular biology techniques (ELISA, RT-PCR). VICs and VECs isolated from patients with AR were characterized and further treated with transforming growth factor (TGF)-β. Anatomically, male had smaller index aortic dimensions and greater AV thickness. Proteome profiler analyzes in AVs (<i>n</i> = 40/sex) evidenced higher expression of inflammatory markers in male and that was further validated (interleukins, chemokines). Histological composition showed higher expression of inflammatory mediators and collagen thick fibers in AVs from male. Male VICs and VECs secreted higher levels of inflammatory markers than female cells. Interestingly, male VICs produced higher amounts of collagen type I and lower fibronectin and aggrecan, whereas male VECs secreted lower decorin. TGF-β exclusively enhanced inflammation in male VICs and decorin and aggrecan in female VICs. Compared with male, AVs from female were thinner, less inflamed, and fibrotic. VICs seem to be the key cell type responsible for the sex-differences. Valvular inflammation associated with an active remodeling process could be a key pathophysiological process involved in AR.<b>NEW & NOTEWORTHY</b> The pathogenesis of chronic aortic regurgitation (AR) is different in male and female. Female patients with AR showed less aortic valve inflammation and collagen accumulation as compared with male. Valvular cells from female patients secreted less inflammatory molecules and collagen and higher levels of proteoglycans. Valvular interstitial cells from females were more sensitive to transforming growth factor (TGF)-β-induced proteoglycans secretion. Our study opens a new perspective oriented toward sex-specific molecular pathways and therapeutic targets in chronic severe AR.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H693-H710"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976991","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":"Enhanced vascular contraction induced by exposure to angiotensin II mediated by endothelin-1 biosynthesis following PKCβ activation.","authors":"Hirotaka Tajima, Nayu Morikita, Masashi Mukohda, Sho Nakamura, Mihiro Seki, Ryuya Imai, Fumiyo Saito, Risuke Mizuno, Hiroshi Ozaki","doi":"10.1152/ajpheart.00541.2024","DOIUrl":"10.1152/ajpheart.00541.2024","url":null,"abstract":"<p><p>Protein kinase C (PKC) reportedly plays a role in the pathogenesis of many vascular dysfunction-related conditions. In this study, we investigated whether PKCβ is associated with vascular contractile changes induced by angiotensin II (Ang II) exposure. Long-term (24 h) treatment of rat aortae and mesenteric arteries in Ang II-containing culture medium enhanced 5-hydroxytryptamine (5-HT)-induced vascular contraction in a dose-dependent manner, in association with enhanced phosphorylation of PKCβ S660. Increased contraction induced by Ang II treatment was also observed in endothelium-denuded aorta. Enhanced contraction induced by Ang II was markedly diminished by the knockout of the PKCβ gene or treatment with LY333531 and CGP53353 (PKCβ inhibitors). Cycloheximide (protein synthesis inhibitor) blocked the Ang II-induced enhanced contraction. Gene expression profiling and real-time PCR analyses showed marked upregulation of endothelin-1 (ET-1) expression in Ang II-treated aorta but was not observed in PKCβ-knockout aorta. Ang II increased the secretion of ET-1 peptide in endothelium-intact and -denuded aortae. Ang II-induced enhancement of vascular contraction was diminished by BQ-123 (ET_AR blocker). In vivo treatment with Ang II (250 ng/kg/min) for 7 days increased phosphorylation of PKCβ S660 in rat vascular tissue and increased the in vitro contractile responses to 5-HT and in vivo systolic blood pressure, but these changes were largely absent in PKCβ-knockout experiments. These data suggest that long-term exposure to Ang II increases vascular smooth muscle contraction and blood pressure elevation, mediated by activation of PKCβ and subsequent biosynthesis of ET-1 in vascular smooth muscle cells.<b>NEW & NOTEWORTHY</b> We studied the role of PKCβ in Ang II-induced hypertension using a rat model. Our study showed that PKCβ plays a key role in Ang II-induced vascular hypercontractility. Our results also suggest that transcriptional activation-mediated ET-1 expression in vascular smooth muscle is responsible for this vascular change as a downstream pathway of PKCβ activation, which leads to blood pressure elevation. This Ang II-PKCβ-ET-1 mechanism may affect vascular homeostasis in hypertension.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H484-H495"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063095","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":"Unveiling hidden dangers: quantitative analysis of ischemic risks in high-risk patients with ASCVD and dyslipidemia.","authors":"Shih-Hsien Sung, Min-Ji Charng","doi":"10.1152/ajpheart.00555.2024","DOIUrl":"10.1152/ajpheart.00555.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H415-H418"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063114","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":"Clinical applications for lipid mediators in STEMI.","authors":"Hiroe Toba, Denan Jin, Shinji Takai","doi":"10.1152/ajpheart.00013.2025","DOIUrl":"10.1152/ajpheart.00013.2025","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H441-H443"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143062989","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}