ArticleJournal of the American Heart Association2022
p53-Dependent Mitochondrial Compensation in Heart Failure With Preserved Ejection Fraction.
Article in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Prospective associations of premature senescence, inflammation, and MERCSs in the cardioprotective effect of CBD in HFpEF.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Article
- Leukocyte telomere length and risk of heart failure with preserved ejection fraction in high-risk Chinese patients with hypertension under 65 years.GeroScience · 2026Observational
- Sub1 contributes to heart failure with preserved ejection fraction driven by aging in mice.Nature communications · 2026Article
- SGLT2 inhibitor dapagliflozin treats heart failure with preserved ejection fraction via the SIRT1/PGC-1α pathway.Acta biochimica et biophysica Sinica · 2026Article
- Article
- Optimized murine HFpEF models for translational preclinical studies.ESC heart failure · 2026Article
- Plasma protein profiles in different heart failure phenotypes.ESC heart failure · 2026Article
- Clinical utility of the four-dimensional automatic left atrial quantification technique in evaluating left atrial volume and function in patients with heart failure with preserved ejection fraction.Quantitative imaging in medicine and surgery · 2026Article
- Variant burden and severity of cardiomyopathy in patients with DMD-related Duchenne muscular dystrophy.Pediatric research · 2026Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- L-GILZ is essential for cardiac function and protects against pressure overload-induced hypertrophy and dysfunction in mice.Asian heart journal · 2025Article
- Circulating mitochondrial DNA signature in cardiometabolic patients.Cardiovascular diabetology · 2025Article
- Mitochondrial Amount Determines Doxorubicin-Induced Cardiotoxicity in Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-cell transcriptomics reveal distinctive patterns of fibroblast activation in heart failure with preserved ejection fraction.Basic research in cardiology · 2024Article
- Doxorubicin-Induced Cardiotoxicity Through SIRT1 Loss Potentiates Overproduction of Exosomes in Cardiomyocytes.International journal of molecular sciences · 2024Article
- Empagliflozin and liraglutide ameliorate HFpEF in mice via augmenting the Erbb4 signaling pathway.Acta pharmacologica Sinica · 2024Article
- Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence.Nucleic acids research · 2024Article
- Biomarkers of Aging and Relevant Evaluation Techniques: A Comprehensive Review.Aging and disease · 2024Review
- Delivery of mitochondria confers cardioprotection through mitochondria replenishment and metabolic compliance.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Heart failure with preserved ejection fraction (HFpEF) accounts for 50% of patients with heart failure. Clinically, HFpEF prevalence shows age and gender biases. Although the majority of patients with HFpEF are elderly, there is an emergence of young patients with HFpEF. A better understanding of the underlying pathogenic mechanism is urgently needed. Here, we aimed to determine the role of aging in the pathogenesis of HFpEF. Methods and Results HFpEF dietary regimen (high-fat diet + Nω-Nitro-L-arginine methyl ester hydrochloride) was used to induce HFpEF in wild type and telomerase RNA knockout mice (second-generation and third-generation telomerase RNA component knockout), an aging murine model. First, both male and female animals develop HFpEF equally. Second, cardiac wall thickening preceded diastolic dysfunction in all HFpEF animals. Third, accelerated HFpEF onset was observed in second-generation telomerase RNA component knockout (at 6 weeks) and third-generation telomerase RNA component knockout (at 4 weeks) compared with wild type (8 weeks). Fourth, we demonstrate that mitochondrial respiration transitioned from compensatory state (normal basal yet loss of maximal respiratory capacity) to dysfunction (loss of both basal and maximal respiratory capacity) in a p53 dosage dependent manner. Last, using myocardial-specific p53 knockout animals, we demonstrate that loss of p53 activation delays the development of HFpEF. Conclusions Here we demonstrate that p53 activation plays a role in the pathogenesis of HFpEF. We show that short telomere animals exhibit a basal level of p53 activation, mitochondria upregulate mtDNA encoded genes as a mean to compensate for blocked mitochondrial biogenesis, and loss of myocardial p53 delays HFpEF onset in high fat diet + Nω-Nitro-L-arginine methyl ester hydrochloride challenged murine model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.