The journal of cardiovascular aging最新文献

{"title":"Current status and global trends in self-care among patients with heart failure: challenges and opportunities.","authors":"Barbara Riegel, Christopher S Lee, Tiny Jaarsma, Anna Stromberg","doi":"10.20517/jca.2026.58","DOIUrl":"10.20517/jca.2026.58","url":null,"abstract":"<p><p>Self-care effectively improves outcomes in adults with chronic conditions such as heart failure (HF). Yet engaging patients in self-care maintenance, self-care monitoring, and self-care management has proven to be difficult for patients and providers. In this review we define self-care as a decision-making process involving the choice of behaviors that maintain physiologic stability and the response to symptoms when they occur. The three core self-care behaviors of maintenance, monitoring, and management are defined and situated within their theoretical context. Available approaches to measurement are described. Details of what is known about self-care maintenance, self-care monitoring, and self-care management from the global literature are synthesized, focusing on efforts to promote HF self-care behaviors and illustrating the challenges experienced by patients. Barriers to and facilitators of HF self-care are described. Hypothesized and known links between HF self-care and pathophysiology such as myocardial stretch, systemic inflammation, neurohormonal activation, and renal function are reviewed. Guidance is provided on how to design effective self-care interventions. Opportunities for future research are described. The article ends with comments on implications for policy to position self-care as a pillar of universal health coverage.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"6 3","pages":"27"},"PeriodicalIF":4.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148922251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Snail-Inspired Metabolic Rewiring Offers a New Avenue to Cardioprotection.","authors":"Xuejun Wang, Neha Dagar","doi":"10.20517/jca.2026.101","DOIUrl":"10.20517/jca.2026.101","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"6 3","pages":"37"},"PeriodicalIF":4.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding cardiovascular aging as a disorder of mitochondrial network.","authors":"Taslima Akter Shila, Dhrubo Ahmad, Jianli Zhao, Huilan Tan, Bo Wang, John Zhang, Yajing Wang","doi":"10.20517/jca.2026.07","DOIUrl":"10.20517/jca.2026.07","url":null,"abstract":"<p><p>Cardiovascular aging is increasingly recognized as a mitochondrial-initiated systemic network dysfunction, a progressive, integrative failure driven by deteriorating mitochondrial quality and signaling. This review synthesizes emerging evidence linking comprehensive mitochondrial pathology to the erosion of cardiovascular resilience as a network-level dysfunction. Age-dependent remodeling of mitochondrial ultrastructure and component composition disrupts respiratory efficiency, positioning bioenergetic insufficiency as a central determinant of reduced stress tolerance across the cardiovascular system. Concurrently, defects in mitochondrial fission-fusion dynamics and impaired mitophagy propagate dysfunction within the mitochondrial network, amplifying the decline in energetic capacity. Beyond energy failure, the release of mitochondrial DNA, vesicles, and peptides activates innate immune sensors such as the cyclic guanosine monophosphate-adenosine monophosphate (GMP-AMP) synthase-stimulator of interferon genes (cGAS-STING) pathway, initiating chronic sterile inflammation that propagates maladaptive remodeling cascades throughout cardiovascular tissues and distal organs. We challenge the traditional view of mitochondria solely as energy producers, revealing that uncoupled perfusion and energy metabolism, together with nitric oxide imbalance, can serve as early indicators of diastolic dysfunction and ischemic susceptibility. Additionally, we introduce the concept of \"mitochondrial age\", a composite measure that integrates respiratory function, imaging-based structural indices, and circulating mitochondrial biomarkers to quantify mitochondrial health. This metric may serve as a translational tool for assessing cardiovascular aging through mitochondrial network communication. Finally, we highlight rejuvenation strategies aimed at restoring mitochondrial youthfulness, ranging from behavioral interventions (exercise, time-restricted feeding) to metabolic and molecular therapies targeting nicotinamide adenine dinucleotide (NAD⁺) metabolism, mitophagy, and endothelial mitochondrial protection. Collectively, this review defines cardiovascular aging as a network-level mitochondrial disorder, offering new conceptual and therapeutic directions for preserving cardiac and vascular function.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"6 2","pages":""},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13521616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148842362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic regulation of cardiac physiology and pathophysiology: biological sex matters.","authors":"Omid M T Rouzbehani, Marta W Szulik, Clint Gwynn, Sophie L Stephens, Riley W Porter, Isidoro Cobo, Manuel Rosa-Garrido, Sarah Franklin, Sihem Boudina","doi":"10.20517/jca.2025.36","DOIUrl":"10.20517/jca.2025.36","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) is the leading cause of global morbidity and mortality, with epigenetic mechanisms playing a pivotal role in its pathogenesis. This review synthesizes current evidence on sex-specific epigenetic regulation in cardiac health and disease, highlighting DNA methylation, histone modifications, and non-coding RNAs as key mediators. Epigenetic processes govern cardiac development, remodeling, and responses to injury, with sex chromosomes, sex hormones, and environmental factors contributing to dimorphic patterns. Developmental programming establishes early sex biases in chromatin architecture while aging and clonal hematopoiesis amplify these differences <i>via</i> mutations in epigenetic modulators. Therapeutic strategies targeting epigenetic regulators hold promise but require sex-tailored approaches to optimize efficacy and minimize off-target effects. This review underscores the critical need for sex-stratified research to advance precision medicine for CVD.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"6 1","pages":""},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13309221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Myocardial Infarction on Cerebral Homeostasis: Exploring the Protective Role of Estrogen.","authors":"Lana El-Samadi, Rana Zahreddine, Joanna A Ziade, Alaa El Ghawi, Ghadir Amin, George W Booz, Fouad A Zouein","doi":"10.20517/jca.2025.02","DOIUrl":"10.20517/jca.2025.02","url":null,"abstract":"<p><p>Myocardial infarction (MI), commonly known as a heart attack, results from the rupture of atherosclerotic plaques in coronary arteries, which triggers a series of pathological events including cardiomyocyte death, thrombus formation, and systemic inflammation. These pathological events lead to significant structural and functional changes in the heart, potentially precipitating heart failure. The ramifications of MI extend beyond cardiac dysfunction and impact cerebral health. Accordingly, this review examines the cerebral implications of MI, focusing on how systemic inflammation and reduced cardiac output post-MI affect cerebral blood flow (CBF) and brain function. MI-induced changes in cardiac output can lead to cerebral hypoperfusion, while neuroinflammation and increased blood-brain barrier (BBB) permeability contribute to cognitive decline and neuronal damage, with potential links to Alzheimer's disease (AD). Furthermore, the review explores the role of estrogen in modulating cardiovascular and cerebral health, particularly in post-menopausal women who exhibit distinct cardiovascular risk profiles. Estrogen protects the heart by regulating local renin-angiotensin-aldosterone systems (RAAS) and has significant impacts on brain function. Declining estrogen levels during menopause exacerbate neuroinflammation and cognitive deficits, highlighting the importance of estrogen in maintaining cerebrovascular function. Experimental studies on estrogen replacement therapies, including 17β-estradiol and selective estrogen receptor modulators (SERMs), show potential in mitigating these detrimental effects, enhancing neurogenesis, and improving cognitive outcomes. Estrogen therapy is crucial in preventing cognitive decline and reducing amyloid plaque formation in Alzheimer's models. This review underscores the potential benefits of estrogen therapy in promoting brain recovery post-MI and improving functional outcomes.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 2","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time's imprint on the left atrium: aging and atrial myopathy.","authors":"Dylan J Gyberg, Ravi B Patel, Michael J Zhang","doi":"10.20517/jca.2024.23","DOIUrl":"10.20517/jca.2024.23","url":null,"abstract":"<p><p>Aging is a primary driver of atrial remodeling and dysfunction, and contributes to the increasing prevalence of atrial myopathy in the aging population. Atrial myopathy, characterized by structural, functional, and electrophysiological abnormalities of the atria, is a key pathological process underlying adverse cardiovascular outcomes such as atrial fibrillation (AF), heart failure with preserved ejection fraction (HFpEF), and ischemic stroke. Although these outcomes are often treated as distinct clinical entities, emerging evidence suggests that they may represent symptomatic manifestations of an underlying atrial disease process. Aging promotes atrial myopathy through multiple mechanisms, including inflammation, extracellular matrix remodeling, electrophysiological alterations, cellular senescence, epigenetic modifications, and non-coding RNA regulation. These changes collectively lead to atrial fibrosis, impaired mechanical function, conduction abnormalities, and a prothrombotic state. Despite its clinical significance, atrial myopathy remains an underrecognized entity, with current management strategies primarily focusing on treating its downstream complications rather than the underlying disease. Advances in imaging techniques, biomarker discovery, and molecular research have the potential to improve the early detection and risk stratification of atrial myopathy, paving the way for novel therapeutic strategies. In this review, we discuss the structural, mechanical, electrophysiological, and metabolic changes that occur in the aging atrium, explore the cellular and molecular mechanisms that drive these changes, and highlight recent advances in diagnostic and therapeutic approaches. By shifting the focus from managing AF and HFpEF to targeting the underlying atrial myopathy, we can unlock new avenues for prevention and treatment, ultimately improving cardiovascular health in the aging population.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 2","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12393009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.","authors":"Sophia A Mahoney, Samuel I Bloom, Douglas R Seals, Anthony J Donato, Matthew J Rossman, Zachary S Clayton","doi":"10.20517/jca.2024.31","DOIUrl":"10.20517/jca.2024.31","url":null,"abstract":"<p><p>Cardiovascular diseases (CVD) remain the leading cause of death worldwide, with advancing age being the primary, nonmodifiable risk factor. Vascular dysfunction, namely arterial stiffening and endothelial dysfunction, is the key antecedent to the development of clinical CVD with aging. Fundamental aging macro-mechanistic processes that drive vascular aging include excess oxidative stress, chronic inflammation, and declines in the vasodilatory molecule nitric oxide. An important hallmark of aging that contributes to the vascular aging processes is cellular senescence - a stress response characterized by cell cycle arrest and accompanied by the production and secretion of proinflammatory molecules (i.e., the senescence-associated secretory phenotype [SASP]). Excess senescent cells and the SASP have deleterious effects on vascular function and in states of CVD, making it a putative therapeutic target for improving vascular function and preventing or reversing CVD. This review will focus on the role of cellular senescence in age-related vascular dysfunction and CVD. We will examine established and emerging mechanisms underlying cellular senescence-induced vascular dysfunction. We will then discuss groups with impaired vascular function and high cellular senescence burden and examine strategies to reduce or remove excess senescent cells and the SASP in the groups who are likely to benefit most from these therapies. Finally, we will highlight the systemic effects of vascular senescent cell suppression on other tissues and organs, given the integrative role of the vasculature in physiology. Together, this review will underscore the imperative role of cellular senescence in vascular dysfunction and the need for a deeper understanding of the translational use of cellular senescence and SASP targeting therapies in groups with high senescent cell burden.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 2","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging triggers mitochondrial, endoplasmic reticulum, and metabolic stress responses in the heart.","authors":"Sakthijothi Muthu, Zinnia Tran, Jayapalraja Thilagavathi, Tanvi Bolarum, Edouard I Azzam, Carolyn K Suzuki, Venkatesh Sundararajan","doi":"10.20517/jca.2024.17","DOIUrl":"10.20517/jca.2024.17","url":null,"abstract":"<p><strong>Introduction: </strong>Aging is a multifaceted biological process characterized by a progressive decline in cellular and tissue function. It significantly impacts the cardiovascular system and contributes to the onset of cardiovascular diseases. The mitochondria (mt) and the endoplasmic reticulum (ER) play synergistic roles in maintaining cellular homeostasis and energy production in the heart. Nevertheless, their response to cardiac aging is not well known.</p><p><strong>Aim: </strong>This study explores mt and ER stress responses and their associated factors, such as metabolic, cellular, and autophagic stress, in cardiac aging.</p><p><strong>Methods and results: </strong>We utilized 10- and 25-month-old CBA/CaJ mice to evaluate mt, ER, and their associated factors, such as metabolic, cellular, and autophagic stress responses. We studied the gene expression for mitochondrial biogenesis, mt and ER stress response, autophagy and metabolic markers, and activating transcription factors that mediate cellular stress responses. We found no significant difference in mtDNA content and the mRNA expression of the mt transcription factor, <i>Tfam</i>; however, selective mtDNA genes, such as <i>mt-Cytb</i> and mt-Co2, showed significant induction in 25-month-aged compared to 10-month-young hearts. Interestingly, genes of several mitochondrial stress response proteases and their components, including <i>Lonp1, Yme1l1, Afg3l2,</i> and <i>Spg7</i>, were significantly induced, with a substantial induction of <i>Clpp</i> and <i>Clpx</i>. However, age-associated differences were not observed in the induction of mt chaperones (<i>Hspa9</i> and <i>Hspd1</i>), but significant induction of <i>Dnaja2</i>, a mitochondrial co-chaperone, was observed. The ER stress transcription factors <i>Xbp1</i> and <i>Atf6</i> were markedly induced in aged hearts, accompanied by decreased expression of ER stress chaperone <i>Hsp90b</i> with no change in <i>Hspa5</i> and <i>Dnajb9</i> chaperones. However, induction of <i>Dnm1l</i> was significant, whereas <i>Mfn1</i> and <i>Fis1</i> were downregulated in contrast to <i>Mfn2</i>, suggesting dysregulated mitochondrial dynamics in the aged heart with no change in autophagy and metabolic stress regulators observed. Furthermore, aged hearts showed significantly increased oxidative damage as evidenced by elevated lipid peroxidation (4-HNE) levels.</p><p><strong>Conclusion: </strong>These findings demonstrate that aging triggers mt, ER, and oxidative stress in the heart, which over time leads to the accumulation of oxidative damage, causing cellular impairment, highlighting these pathways as potential therapeutic targets for mitigating age-related cardiac dysfunction.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Declining nitric oxide bioavailability in cardiovascular aging: mechanistic insights and emerging interventions.","authors":"Hriju Adhikari, Priyanka Patel, Namratha Javvaji, Mark J Crabtree, Jillian N Simon","doi":"10.20517/jca.2025.14","DOIUrl":"10.20517/jca.2025.14","url":null,"abstract":"<p><p>Nitric oxide (NO) is essential for maintaining normal cardiovascular function, and accumulating evidence suggests that its diminished bioavailability contributes to endothelial dysfunction, vascular stiffening, and impaired cardiac performance - hallmarks of cardiovascular aging. This review posits that reduced NO bioavailability with age stems from impaired endothelial and neuronal NO synthase activity, increased oxidative stress, and metabolic shifts that drive cardiovascular decline. We further discuss emerging research which highlights potential interventions, including dietary nitrate supplementation, caloric restriction, and exercise, that may restore NO signaling and counteract age-related cardiovascular dysfunction. These findings underscore the growing recognition of NO as a key regulator of cardiovascular aging and a promising therapeutic target. Addressing NO-related deficits could open new avenues for preventing and treating age-associated cardiovascular diseases, reshaping strategies for promoting healthy aging and longevity.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 4","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13055925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147640822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of plasminogen activator inhibitor-1 (PAI-1) in age-related cardiovascular pathophysiology.","authors":"Alireza Khoddam, Douglas Vaughan, Lisa Wilsbacher","doi":"10.20517/jca.2024.38","DOIUrl":"10.20517/jca.2024.38","url":null,"abstract":"<p><p>Cardiovascular aging underpins the development of age-related diseases, including heart failure and vascular dysfunction, and is driven by molecular and cellular mechanisms described in the hallmarks of aging. Plasminogen activator inhibitor-1 (PAI-1), a key regulator of fibrinolysis, also mediates processes like vascular stiffness, cellular senescence, and immune evasion. This review highlights PAI-1's role in cardiovascular aging with a special emphasis on senescence, a key hallmark of aging. It further explores PAI-1's therapeutic potential, with a focus on its contribution to ECM remodeling, senescence signaling, and immune checkpoint regulation. Targeting PAI-1 could provide a promising strategy to mitigate age-related cardiovascular disease.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":"5 2","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12919670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147273490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}