Articles
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ChatGPT and other artificial intelligence chatbots and biomedical writing
J Cardiovasc Aging 2023;3:20. DOI: 10.20517/jca.2023.13Editorial|Published on: 31 Mar 2023 -
CaMKIIδ gene editing - A base hit for the heart
J Cardiovasc Aging 2023;3:19. DOI: 10.20517/jca.2023.11Commentary|Published on: 22 Mar 2023 -
Exercise induces cardiomyogenesis in the aged heart
J Cardiovasc Aging 2023;3:18. DOI: 10.20517/jca.2023.06Commentary|Published on: 14 Mar 2023 -
Immune mechanisms of cardiac aging
J Cardiovasc Aging 2023;3:17. DOI: 10.20517/jca.2023.02AbstractAdvances in healthcare and improvements in living conditions have led to rising life expectancy worldwide. ... MOREAdvances in healthcare and improvements in living conditions have led to rising life expectancy worldwide. Aging is associated with excessive oxidative stress, a chronic inflammatory state, and limited tissue healing, all of which result in an increased risk of heart failure. In fact, the prevalence of heart failure approaches 40% in the ninth decade of life, with the majority of these cases suffering from heart failure with preserved ejection fraction (HFpEF). In cardiomyocytes (CMs), age-related mitochondrial dysfunction results in disrupted calcium signaling and covalent protein-linked aggregates, which cause cardiomyocyte functional disturbances, resulting in increased stiffness and diastolic dysfunction. Importantly, aging is also associated with chronic low-grade, sterile inflammation, which alters the function of interstitial cardiac cells and leads to cardiac fibrosis. Taken together, cardiac aging is associated with cellular, structural, and functional changes in the heart that contribute to the rising prevalence of heart failure in older people. LESS Full articleReview|Published on: 9 Mar 2023 -
Protein homeostasis in the aged and diseased heart
J Cardiovasc Aging 2023;3:16. DOI: 10.20517/jca.2023.4AbstractProtein homeostasis, the balance between protein synthesis and degradation, requires the clearance of misfolded and ... MOREProtein homeostasis, the balance between protein synthesis and degradation, requires the clearance of misfolded and aggregated proteins and is therefore considered to be an essential aspect of establishing a physiologically effective proteome. Aging alters this balance, termed “proteostasis”, resulting in the progressive accumulation of misfolded and aggregated proteins. Defective proteostasis leads to the functional deterioration of diverse regulatory processes during aging and is implicated in the etiology of multiple pathological conditions underlying a variety of neurodegenerative diseases and in age-dependent cardiovascular disease. Detergent-insoluble protein aggregates have been reported by us in both aged and hypertensive hearts. The protein constituents were found to overlap with protein aggregates seen in neurodegenerative diseases such as Alzheimer’s disease. Therefore, targeting these protein components of aggregates may be a promising therapeutic strategy for cardiovascular pathologies associated with aging, ischemia, and/or hypertension. LESS Full articleReview|Published on: 7 Mar 2023 -
ASGR1 and cholesterol: connecting the dots
J Cardiovasc Aging 2023;3:15. DOI: 10.20517/jca.2023.8Commentary|Published on: 6 Mar 2023 -
Can age be a modifiable risk factor? the impact of dietary patterns on the molecular mechanisms that underlie cardiovascular aging
J Cardiovasc Aging 2023;3:14. DOI: 10.20517/jca.2023.1AbstractAging is the number one risk factor for the development of cardiovascular disease (CVD). Therefore, ... MOREAging is the number one risk factor for the development of cardiovascular disease (CVD). Therefore, an evaluation of therapies for the prevention of CVD should focus on factors that slow down aging, particularly cardiovascular aging. There are various proposed mechanisms that advance cardiovascular age; in this review, we focus on chronic inflammation, oxidative stress and epigenetics as the primary drivers of aging. Furthermore, we will evaluate several dietary patterns on their impact on these aging mechanisms. The traditional "heart-healthy" dietary patterns such as the Mediterranean diet, plant-based diet and intermittent fasting will be evaluated for their performance to slow down the aforementioned aging mechanisms. The aim of this review will be to guide practitioners and patients on the dietary components that can slow down the effects of aging to prevent CVD. LESS Full articleReview|Published on: 1 Mar 2023 -
Reassessment of genes associated with dilated and hypertrophic cardiomyopathy in a Chinese Han population
J Cardiovasc Aging 2023;3:12. DOI: 10.20517/jca.2022.44AbstractIntroduction: More than 100 genes are reportedly associated with dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy ... MOREIntroduction: More than 100 genes are reportedly associated with dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). However, the situation that many genes lack of reassessment in a large population hinders the interpretations of these genes in genetic diagnostic testing. Moreover, limited genetic data for cardiomyopathy in Chinese patients was reported.Aim: Therefore, here we reassessed an estimated 500 putative genes in the Chinese Han population by whole exome sequencing (WES) to describe the landscape of variants in these genes and to confirm their genetic contribution to DCM and HCM.Methods and Results: WES was performed in 1059 DCM patients, 1175 HCM patients and 514 controls. Approximately 500 candidate genes were selected for evaluation. Truncating variants of TTN and MYBPC3 were the most burdensome for both groups. Gene-based association tests identified 35 and 35 genes associated with DCM and HCM, respectively. Except for the known genes of cardiomyopathy, the top three genes associated with DCM were MUC16, KMT2C, and FBN1, while the top three genes associated with HCM were KMT2C, RYR2, and SCN5A. After filtering for pathogenicity, FBN1 is still significantly associated with DCM and SCN5A and RYR2 remains significantly enriched in HCM patients. However, after adjustment, only TTN with DCM and MYBPC3 and MYH7 with HCM remains significant.Conclusion: We described the genetic landscape of Chinese patients with DCM and HCM and developed a website (www.cardioexome.cn) to enable open access to this information. Furthermore, the gene-based association test confirmed the contribution of TTN to DCM and MYBPC3 and MYH7 to HCM in Chinese Han. In addition, the website, www.cardioexome.cn, was developed to store these sequencing results. LESS Full articleOriginal Research Article|Published on: 10 Feb 2023 -
What ails the NIH peer review study sections and how to fix the review process of the grant applications
J Cardiovasc Aging 2023;3:11. DOI: 10.20517/jca.2023.3Perspective|Published on: 16 Jan 2023 -
Parsing cell death in arrhythmogenic cardiomyopathy: PANoptosis
J Cardiovasc Aging 2023;3:10. DOI: 10.20517/jca.2022.45Editorial|Published on: 12 Jan 2023
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Epigenetic dysregulation in cardiovascular aging and disease
J Cardiovasc Aging 2021;1:10. DOI: 10.20517/jca.2021.16AbstractCardiovascular disease (CVD) is the leading cause of mortality and morbidity for all sexes, racial ... MORECardiovascular disease (CVD) is the leading cause of mortality and morbidity for all sexes, racial and ethnic groups. Age, and its associated physiological and pathological consequences, exacerbate CVD incidence and progression, while modulation of biological age with interventions track with cardiovascular health. Despite the strong link between aging and CVD, surprisingly few studies have directly investigated heart failure and vascular dysfunction in aged models and subjects. Nevertheless, strong correlations have been found between heart disease, atherosclerosis, hypertension, fibrosis, and regeneration efficiency with senescent cell burden and its proinflammatory sequelae. In agreement, senotherapeutics have had success in reducing the detrimental effects in experimental models of cardiovascular aging and disease. Aside from senotherapeutics, cellular reprogramming strategies targeting epigenetic enzymes remain an unexplored yet viable option for reversing or delaying CVD. Epigenetic alterations comprising local and global changes in DNA and histone modifications, transcription factor binding, disorganization of the nuclear lamina, and misfolding of the genome are hallmarks of aging. Limited studies in the aging cardiovascular system of murine models or human patient samples have identified strong correlations between the epigenome, age, and senescence. Here, we compile the findings in published studies linking epigenetic changes to CVD and identify clear themes of epigenetic deregulation during aging. Pending direct investigation of these general mechanisms in aged tissues, this review predicts that future work will establish epigenetic rejuvenation as a potent method to delay CVD. LESS Full articleReview|Published on: 23 Aug 2021 -
Editors’ Preamble to The Journal of Cardiovascular Aging
J Cardiovasc Aging 2021;1:1. DOI: 10.20517/jca.2021.01Editorial|Published on: 27 Apr 2021 -
Ser9 phosphorylation of GSK-3β promotes aging in the heart through suppression of autophagy
J Cardiovasc Aging 2021;1:9. DOI: 10.20517/jca.2021.13AbstractIntroduction: Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine kinase and a negative regulator of cardiac ... MOREIntroduction: Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine kinase and a negative regulator of cardiac hypertrophy. Phosphorylation of GSK-3β at Ser9 negatively regulates its kinase activity. The role of GSK-3β in cardiac aging remains poorly understood.Aim: The study aimed to elucidate the role of GSK-3β Ser9 phosphorylation in mediating cardiac aging and the underlying mechanism.Methods and Results: Phosphorylation of GSK-3β at Ser9 and the levels of β-catenin and Mcl-1 were increased in the mouse heart during aging, suggesting that GSK-3β is inactivated during aging in the heart. Age-induced cardiac hypertrophy, fibrosis, left ventricular dysfunction, and increases in cardiomyocyte apoptosis and senescence were all attenuated in constitutively active GSK-3βS9A knock-in (KI) mice compared to littermate wild type mice. Although autophagy is inhibited in the heart during aging, KI of GSK-3βS9A reversed the age-associated decline in autophagy in the mouse heart. GSK-3β directly phosphorylates Ulk1, a regulator of autophagy, at Ser913, thereby stimulating autophagy in cardiomyocytes. Ulk1Ser913A KI mice exhibited decreased autophagic flux and increased senescence in cardiomyocytes.Conclusion: Our results suggest that GSK-3β is inactivated during aging through Ser9 phosphorylation, which in turn plays an important role in mediating cardiac aging. GSK-3β promotes autophagy through phosphorylation of Ulk1 at Ser913, which in turn prevents aging in the heart.One sentence summary: Ser9 phosphorylation of GSK-3β promotes aging in the heart at least in part through decreases in Ulk1 phosphorylation at Ser913 and suppression of autophagy. LESS Full articleOriginal Research Article|Published on: 23 Aug 2021 -
Adenine base editing to treat progeria syndrome and extend the lifespan
J Cardiovasc Aging 2021;1:8. DOI: 10.20517/jca.2021.10Commentary|Published on: 17 Jun 2021 -
S-nitrosoglutathione reductase (GSNOR) deficiency accelerates cardiomyocyte differentiation of induced pluripotent stem cells
J Cardiovasc Aging 2021;1:13. DOI: 10.20517/jca.2021.19AbstractIntroduction: Induced pluripotent stem cells (iPSCs) provide a model of cardiomyocyte (CM) maturation. Nitric oxide ... MOREIntroduction: Induced pluripotent stem cells (iPSCs) provide a model of cardiomyocyte (CM) maturation. Nitric oxide signaling promotes CM differentiation and maturation, although the mechanisms remain controversial.Aim: The study tested the hypothesis that in the absence of S-nitrosoglutathione reductase (GSNOR), a denitrosylase regulating protein S-nitrosylation, the resultant increased S-nitrosylation accelerates the differentiation and maturation of iPSC-derived cardiomyocytes (CMs).Methods and Results: iPSCs derived from mice lacking GSNOR (iPSCGSNOR-/-) matured faster than wildtype iPSCs (iPSCWT) and demonstrated transient increases in expression of murine Snail Family Transcriptional Repressor 1 gene (Snail), murine Snail Family Transcriptional Repressor 2 gene (Slug) and murine Twist Family BHLH Transcription Factor 1 gene (Twist), transcription factors that promote epithelial-to-mesenchymal transition (EMT) and that are regulated by Glycogen Synthase Kinase 3 Beta (GSK3β). Murine Glycogen Synthase Kinase 3 Beta(Gsk3β) gene exhibited much greater S-nitrosylation, but lower expression in iPSCGSNOR-/-. S-nitrosoglutathione (GSNO)-treated iPSCWT and human (h)iPSCs also demonstrated reduced expression of GSK3β. Nkx2.5 expression, a CM marker, was increased in iPSCGSNOR-/- upon directed differentiation toward CMs on Day 4, whereas murine Brachyury (t), Isl1, and GATA Binding Protein(Gata4) mRNA were decreased, compared to iPSCWT, suggesting that GSNOR deficiency promotes CM differentiation beginning immediately following cell adherence to the culture dish-transitioning from mesoderm to cardiac progenitor.Conclusion: Together these findings suggest that increased S-nitrosylation of Gsk3β promotes CM differentiation and maturation from iPSCs. Manipulating the post-translational modification of GSK3β may provide an important translational target and offers new insight into understanding of CM differentiation from pluripotent stem cells.One sentence summary: Deficiency of GSNOR or addition of GSNO accelerates early differentiation and maturation of iPSC-cardiomyocytes. LESS Full articleOriginal Research Article|Published on: 7 Sep 2021
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Promoting healthy cardiovascular aging: emerging topics
Review|Published on: 29 Jul 2022 -
Cancer treatment-induced NAD+ depletion in premature senescence and late cardiovascular complications
Review|Published on: 29 Apr 2022 -
Metabolic targets in cardiac aging and rejuvenation
Review|Published on: 14 Sep 2022 -
Gut microbiota in sarcopenia and heart failure
Review|Published on: 5 Jul 2022 -
STEMIN and YAP5SA synthetic modified mRNAs regenerate and repair infarcted mouse hearts
Original Research Article|Published on: 15 Jun 2022
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PANoptosis is a prominent feature of desmoplakin cardiomyopathy
Original Research Article|Published on: 1 Jan 2023 -
The importance of “when” in calorie restriction-induced lifespan extension
Commentary|Published on: 1 Jan 2023 -
The role of paracrine crosstalk between myeloid and endothelial cells in myocardial angiogenesis and infarcted heart repair
Commentary|Published on: 1 Jan 2023 -
New insights into the dynamics of age-related clonal hematopoiesis
Commentary|Published on: 1 Jan 2023
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About The Journal
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ISSN
2768-5993 (Online)
Publisher
OAE Publishing Inc.
Article Processing Charges
$1200
Manuscript Processing Cycle (peer reviewed only)
Time from submission to first decision: 18 days (4-38 days)
Time from submission to publication: 31 days (12-48 days)
(not include the time that authors spend on revision)
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Editor-in-Chief
Ali J. Marian
Publishing Model
Gold Open Access
Copyright
Copyright is retained by author(s)
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Publication Frequency
Quarterly
Indexing
Open Archives
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Portico
All published articles are preserved here permanently:
https://www.portico.org/publishers/oae/