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

{"title":"Multi-Omics Approaches to Cardiovascular Disease: Technological Innovations and Clinical Translation.","authors":"Binte Zehra, Nidhina Vinod, Shuhd BinEshaq, Inna Aleksandrova, Richa Tambi, Muhammed Faizan, Samah Alasrawi, Mohamed Almarri, Martina Brueckner, Wolfgang M Kuebler, Wendy K Chung, Sumaya Almansoori, Roberto M Di Donato, Mohammed Uddin, Stefan S Du Plessis, Alawi Alsheikh-Ali, Bakhrom K Berdiev","doi":"10.1152/ajpheart.00024.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00024.2026","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain the leading cause of global morbidity and mortality, reflecting a persistent gap between clinical phenotyping and the molecular mechanisms that govern disease initiation, progression, and inter-individual variability. Recent advances in emerging technologies have fundamentally reshaped cardiovascular physiology by enabling high-resolution, cross-layer profiling of the heart and vasculature across genomic, epigenomic, transcriptomic, proteomic, metabolomic, lipidomic, glycomic, and fluxomic layers, increasingly at single-cell and spatial resolution. These approaches reveal CVD as a coordinated, multi-layered process driven by dynamic interactions among cell types, regulatory programs, and metabolic states, rather than isolated gene-level defects. In this review, we synthesize how emerging multi-omic, computational, and functional genomics technologies are redefining the study of cardiovascular disease across molecular, cellular, and tissue levels. We highlight recent innovations in single-cell and spatial atlases, long-read sequencing, proteomics and metabolomics, integrative data modeling, and functional omics approaches, including genome-scale perturbation screens and single-cell perturbation frameworks. These platforms enable mechanistic dissection of regulatory circuits, distinguish primary disease drivers from secondary adaptations, and directly assess therapeutic reversibility, advancing the field beyond associative biomarker discovery toward mechanism-guided target prioritization. We further discuss key methodological and translational challenges accompanying high-dimensional cardiovascular data, including pre-analytical variability, control selection, temporal misalignment across molecular layers, population diversity and reference bias. By integrating technological innovation with computational rigor and functional validation, this review frames emerging omics-enabled strategies as a unified, physiologically grounded framework for translating molecular insight into clinically meaningful cardiovascular phenotypes and advancing precision cardiovascular medicine.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759953","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":"Methodological approaches and the clinical utility of non-invasive estimated pulse wave velocity.","authors":"James R Cox, Farhan Ahmed, Catherine Liao, Alberto P Avolio, Ahmad Qasem, Mark Butlin","doi":"10.1152/ajpheart.00823.2025","DOIUrl":"https://doi.org/10.1152/ajpheart.00823.2025","url":null,"abstract":"<p><p><i><b>Background.</b></i> Arterial stiffness, as measured by carotid-femoral pulse wave velocity (cfPWV), is an independent cardiovascular risk factor. Arterial stiffness measurement requires the acquisition of pulse waveforms at two arterial sites. This technique is often constrained to clinical or laboratory settings. Estimated PWV (ePWV) addresses these limitations by only requiring the measurement of a single pulse, or no pulse at all, providing a wider application for cardiovascular health monitoring. The aim of this systematic literature review is to investigate the various approaches and clinical utility of ePWV as a surrogate measure of arterial stiffness. <i><b>Methodology.</b></i> The literature search followed the PRISMA guidelines and was conducted in the following databases: Embase; MEDLINE; PubMed; and Scopus. <i><b>Results.</b></i> The initial search identified 409 papers: Embase (n = 38); MEDLINE (n = 98); PubMed (n = 93); and Scopus (n = 180). After screening and applying the exclusion criteria 131 eligible papers remained. Peak topic publication occurred in 2024 (30%). Most papers (69%) employed regression-based approaches in ePWV whilst 34% employed a pulse wave analysis (PWA)-based approach. Most PWA approaches (57%) used an oscillometric cuff. There were few validation studies (12%). Validation studies presented correlations (r) from 0.35 to 0.92 and standard deviations reaching ±2.54 m/s. <i><b>Conclusion.</b></i> The use of ePWV as a surrogate for arterial stiffness is positively observed across the literature. However, validation studies reveal substantial individual differences hidden within acceptable population averages, underscoring the need to refine estimation algorithms for greater precision.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147715657","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":"Postnatal upregulation of cyclooxygenase-2 (COX-2) drives anatomical closure of the ductus arteriosus.","authors":"Takashi Noguchi, Yuko Hidaka, Sayuki Oka, Takahiro Kemmotsu, Yuna Takeuchi, Toshihiro Nakayama, Kenji Yoshida, Takashi Nakamura, Keiko Uchida, Etsuko Miyagi, Utako Yokoyama","doi":"10.1152/ajpheart.00647.2025","DOIUrl":"10.1152/ajpheart.00647.2025","url":null,"abstract":"<p><p>Postnatal environmental changes markedly facilitate functional closure of the ductus arteriosus (DA). Vascular remodeling during both fetal and postnatal periods is essential for achieving permanent anatomical DA closure; however, molecular mechanisms driving postnatal DA remodeling have yet to be fully elucidated. Single-cell RNA sequencing (scRNA-seq) revealed that postnatal mouse smooth muscle cells (SMCs) formed a transcriptionally distinct cluster compared with fetal ductus arteriosus smooth muscle cells (DASMCs), whereas other cell types remained in the same cluster after birth, highlighting a critical role for SMCs in postnatal DA remodeling. Transcriptome analysis identified genes differentially expressed in postnatal DASMCs compared with the adjacent arteries, among which cyclooxygenase-2 (COX-2) exhibited the most robust induction. Exposure to hydrogen peroxide, simulating oxidative stress encountered after birth, significantly increased COX-2 mRNA and protein expression in DASMCs. Given that platelet adhesion is a postnatal event in the DA and platelets are a major source of thromboxane A₂, we administered thromboxane A₂ receptor agonist to DASMCs and found marked COX-2 upregulation. Lentiviral-based overexpression of COX-2 led to prostaglandin E₂ (PGE₂) production. PGE₂ stimulation increased expression of <i>Nr4a1</i> via PGE₂ receptor EP4. <i>Nr4a1</i> silencing inhibited DASMC proliferation. To assess the in vivo relevance of COX-2, we maternally administered a selective COX-2 inhibitor, SC-236, and found impaired postnatal DA closure in mice. These data suggest that postnatal upregulation of COX-2 in DASMCs promotes anatomical closure, potentially involving <i>Nr4a1</i>; inhibition of COX-2 at the very early postnatal period may interfere with DA closure.<b>NEW & NOTEWORTHY</b> Postnatal environmental changes promote anatomical closure of the ductus arteriosus (DA). This study identifies cyclooxygenase-2 (COX-2) as a key driver of postnatal DA remodeling. DA smooth muscle cells (SMCs) undergo transcriptional changes after birth, with COX-2 markedly upregulated by oxidative stress and thromboxane A₂. COX-2-derived prostaglandin E₂ enhanced SMC proliferation, potentially involving <i>Nr4a1</i>. In vivo COX-2 inhibition impaired DA closure, highlighting its essential role and potential vulnerability to early postnatal COX-2 suppression.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H996-H1011"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147275733","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 implications of azygos venous flow assessment in patients with interrupted inferior vena cava undergoing Fontan completion.","authors":"Sercin Ozkok, Yigit Can Kartal, Hakan Ayyıldız","doi":"10.1152/ajpheart.00021.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00021.2026","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"330 4","pages":"H1257-H1258"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147626492","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":"QT interval and cardiac restitution dynamics in racehorses: observations during maximal effort.","authors":"Amanda Avison, W Glen Pyle, William Sears, Peter W Physick-Sheard","doi":"10.1152/ajpheart.00785.2025","DOIUrl":"10.1152/ajpheart.00785.2025","url":null,"abstract":"<p><p>Sudden cardiac death is a leading cause of athletic death in both humans and horses, making racehorses a potentially valuable model for investigating sudden cardiac death. Cardiac restitution ratio (QT/TQ interval) is used to assess arrhythmia risk in humans, but investigations in athletes are scarce. The objective was to characterize the QT interval and cardiac restitution ratio in Thoroughbred racehorses during maximal effort. Automated restitution analysis was performed using 2,709 pairs of cardiac cycles from 30 Thoroughbred horses during races. Cardiac cycles were obtained during: prerace; acceleration out of the gate; race; immediate postrace; and recovery phases. Multivariable linear regression analyses were performed with both QT interval and cardiac restitution ratio as outcomes of interest. The QT/RR relationship varied by exercise period with cycles during maximal effort being distinct from those of prerace and recovery periods. Exercise period, RR interval, and their interaction were significantly associated with both QT interval and cardiac restitution ratio during maximal effort. QT intervals during the postrace period were relatively unresponsive to changes in RR interval compared with other exercise periods. QT intervals were longer, and cardiac restitution ratio were higher prerace than recovery at the same RR intervals. The QT/RR relationship is multifactorial, and variables associated with QT interval during maximal effort differ from other exercise periods. These changes suggest differences in intracellular mechanisms and/or extracellular controls (e.g., autonomic activity) between exercise periods that have biologically significant effects on myocardial electrophysiology and pathophysiology. Racehorses may be a useful model for studying cardiac function during exercise.<b>NEW & NOTEWORTHY</b> ECG recordings obtained from racehorses during competition provide insight into the cardiac physiology of athletes and potentially pathophysiologic mechanisms that underlie the risk of exercise-associated arrhythmias. The QT/RR relationship is uniquely altered during maximal effort compared with other exercise periods, and the response of the QT interval to changes in heart rate (RR interval) is decreased immediately postrace.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1211-H1221"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353321","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":"Genetic diversity and molecular mechanisms in hypertrophic cardiomyopathy: toward personalized therapy.","authors":"Komal Marwaha, Behram Mody, Nathan Holland, Mariela Lane, Brittany D Shoemake, Namrata Singh, Freny Vaghaiwalla Mody","doi":"10.1152/ajpheart.00500.2025","DOIUrl":"10.1152/ajpheart.00500.2025","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac muscle disorder, yet contemporary genomic and mechanistic research still lacks a cohesive model explaining how diverse genetic architectures give rise to heterogeneous phenotypes. This review synthesizes advances across sarcomeric and nonsarcomeric mutations, including intermediate-effect variants, polygenic modifiers, and ancestry-dependent sources of variant misclassification to elucidate how these factors govern disease penetrance and clinical expression. It critically evaluates how genetic diversity intersects with key molecular pathways, including sarcomeric hypercontractility, calcium dysregulation, mitochondrial energy deficiency, and transforming growth factor-β (TGF-β) and protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling, to drive hypertrophic and fibrotic remodeling. Emerging mechanism-based therapies, such as myosin inhibition, allele-specific silencing, clustered regularly interspaced short palindromic repeats (CRISPR)-based correction, and metabolic modulation, are examined with respect to their capacity to modify upstream molecular drivers rather than downstream hemodynamic consequences. Persistent challenges, including variants of uncertain significance classification, ancestry-biased databases, inequitable access to genetic testing, and unresolved safety concerns for gene-based therapies, are critically assessed as major barriers to precision-medicine integration. By linking genetic architecture, molecular pathogenesis, and targeted interventions, this review advances a contemporary, mechanistically grounded framework that informs both individualized management and future research directions. Future research should prioritize pathway-specific therapeutics, functional and mechanistic validation of emerging variants, deeper physiologic phenotyping to refine disease modeling, and accelerate translation throughout the continuum of HCM pathophysiology.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"330 4","pages":"H1073-H1091"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497318","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":"NAV3 as a novel and master regulator of cardiac fibrosis.","authors":"Prasanth Puthanveetil","doi":"10.1152/ajpheart.00173.2026","DOIUrl":"10.1152/ajpheart.00173.2026","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1239-H1240"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472457","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":"Sympathetic neural control of blood pressure across the premenopausal lifespan.","authors":"Jinan Saboune, Natasha G Boyes, Jacqueline K Limberg, Charlotte W Usselman","doi":"10.1152/ajpheart.00739.2025","DOIUrl":"10.1152/ajpheart.00739.2025","url":null,"abstract":"<p><p>The technique of microneurography has advanced our understanding of the sympathetic nervous system's role in the neurovascular control of blood pressure in humans, yet critical knowledge gaps remain, particularly across the premenopausal female lifespan. Historically, premenopausal females have been considered relatively protected from cardiovascular diseases, leading to a disproportionate focus on postmenopausal populations in cardiovascular research. However, emerging evidence contradicts this assumption: premenopausal females with hypertension exhibit 15-20% higher mortality rates than age-matched males, and myocardial infarction deaths are rising fastest among females under the age of 45. This review addresses a major void in the literature by examining sympathetic regulation of blood pressure in premenopausal females and how it is modulated across unique reproductive health states, including menstrual cycling, hormonal contraceptive use, pregnancy, polycystic ovary syndrome, uterine fibroids, and endometriosis. Muscle sympathetic nerve activity fluctuates with some but not all hormonal changes, depending on the population and the conditions under which they are studied. Moreover, corresponding effects on blood pressure vary widely, suggesting a high degree of variability in how sympathetic outflow is transduced into blood pressure in females. Overall, our review highlights the need for longitudinal and mechanistic studies focused on hormonal transitions and specific premenopausal health states to better understand, and eventually mitigate, female-specific cardiovascular risk.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1340-H1357"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353334","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":"Elevated asprosin in postmenopause is associated with vasculometabolic complications.","authors":"Nefia Chacko, Mohit Shah, Reia Thomas, Christian Jude-Aspiras, Akinobu Watanabe, Maria Alicia Carrillo-Sepulveda","doi":"10.1152/ajpheart.00042.2026","DOIUrl":"10.1152/ajpheart.00042.2026","url":null,"abstract":"<p><p>Postmenopause is associated with increased adiposity, metabolic syndrome, and heightened cardiovascular disease (CVD) risk, yet the adipose-derived factors potentially contributing to vascular impairment remain poorly defined. Asprosin, a glucogenic adipokine secreted by white adipose tissue (WAT), is elevated in metabolic diseases; however, its association with postmenopausal vascular complications remains unknown. In this study, we investigated circulating and adipose tissue asprosin levels in a long-term ovariectomy (OVX) mouse model of postmenopause. Female mice underwent OVX or sham surgery and were followed for 20 wk. OVX mice developed typical postmenopausal bone porosity, specifically in the lumbar vertebrae, along with cardiometabolic disorders, including weight gain, increased adiposity, metabolic syndrome-like alterations, and significant arterial stiffness, an early vascular insult marker. Notably, these postmenopausal changes were associated with elevated circulating asprosin levels and increased asprosin expression in subcutaneous adipose tissue. Results from ex vivo wire myography studies demonstrated that asprosin directly potentiates vasoconstriction, implying that asprosin exerts a direct vascular effect. Together, these findings provide novel evidence of an association between elevated asprosin and postmenopausal vasculometabolic alterations. These observations support further investigation of asprosin as a potential biomarker of cardiometabolic and vascular changes and as a candidate for future investigation.<b>NEW & NOTEWORTHY</b> Postmenopause is a critical period in women's lives marked by metabolic and vascular changes that remain poorly understood. Asprosin, a novel adipokine, is linked to metabolic disorders and cardiovascular risk. In long-term OVX mice, circulating asprosin levels were elevated and associated with weight gain and arterial stiffness. Exogenous asprosin was associated with vasoconstriction, supporting its potential as a biomarker and a candidate for further mechanistic investigation in postmenopausal vasculometabolic regulation.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1293-H1301"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472420","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":"Lack of endothelial estrogen receptor alpha signaling exacerbates abdominal aortic aneurysm in male mice.","authors":"Neekun Sharma, Yijin Huang, Guanghong Jia, Luis A Martinez-Lemus, Jaume Padilla, Camila Manrique-Acevedo","doi":"10.1152/ajpheart.00085.2026","DOIUrl":"10.1152/ajpheart.00085.2026","url":null,"abstract":"<p><p>Abdominal aortic aneurysm (AAA), a pathological dilatation of the abdominal aorta, is primarily driven by chronic inflammation of the aortic wall. Although estrogen is known to exert protective anti-inflammatory effects in AAA, the role of endothelial estrogen receptor alpha (ERα) signaling in AAA pathogenesis remains unclear. We investigated the vasoprotective role of endothelial ERα using endothelial cell (EC)-specific ERα knockout (eERαKO) mice subjected to a beta-aminopropionitrile plus angiotensin II model of AAA. eERα deficiency significantly accelerated AAA formation in male mice, evidenced by increased maximal aortic diameter, worsened medial elastin degradation, increased collagen deposition, and upregulated macrophage infiltration, whereas female mice were largely unaffected. Mechanistically, loss of endothelial ERα was associated with elevated endothelin-1 (ET-1) expression in aortic tissue. In vitro, pharmacological inhibition of ERα with methyl-piperidino-pyrazole increased endothelial ET-1 secretion and increased monocyte adhesion in EC-monocyte coculture assays. Collectively, these findings reveal that endothelial ERα constrains AAA development in male mice, possibly by suppressing ET-1-mediated endothelial activation and macrophage recruitment. This work highlights a protective role of endothelial ERα signaling in maintaining aortic structural integrity and preventing aneurysmal disease.<b>NEW & NOTEWORTHY</b> We identify an important role of endothelial estrogen receptor alpha (ERα) in a sex-dependent regulation of abdominal aortic aneurysm formation. Using mice with endothelial cell-specific deletion of ERα, we found that loss of endothelial ERα signaling exacerbates aneurysm development in male mice, associated with increased macrophage infiltration and elevated endothelin-1 expression. These findings reveal a previously unrecognized endothelial-specific mechanism by which estrogen signaling preserves aortic wall integrity and suppresses inflammatory vascular remodeling.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1319-H1327"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147455230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}