ArticleInternational journal of molecular sciences2019
Loss of Apelin Augments Angiotensin II-Induced Cardiac Dysfunction and Pathological Remodeling.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- The Apelin-APJ Axis in Heart Failure: Mechanistic Insights, Clinical Evidence, and Translational Challenges.Cardiovascular drugs and therapy · 2026Review
- Review
- The Apelinergic System in Kidney Disease: Novel Perspectives.International journal of molecular sciences · 2025Review
- Beyond Leptin and Adiponectin: The Diverse Roles of Adipokines in the Myocardial Hypertrophic Process and Heart Failure and Their Potential Contribution in Obesity.International journal of molecular sciences · 2025Review
- A biodegradable, microstructured, electroconductive and nano-integrated drug eluting patch (MENDEP) for myocardial tissue engineering.Bioactive materials · 2025Article
- Novel insights into the central protective role of ACE2 in diabetic cardiomyopathy: from underlying signaling pathways to therapeutic perspectives.Molecular and cellular biochemistry · 2025Review
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Article
- Gene expression profiles, potential targets and treatments of cardiac remodeling.Molecular and cellular biochemistry · 2025Review
- Article
- Investigation of Genetic Variations in APLN and APLNR Genes and Their Potential Role in Cardiovascular Diseases.Reports of biochemistry & molecular biology · 2025Article
- The Apelin/APJ System: A Potential Therapeutic Target for Sepsis.Journal of inflammation research · 2024Review
- Protective effects of limb remote ischemic per-conditioning on the heart injury induced by renal ischemic-reperfusion through the interaction of the apelin with the RAS/iNOS pathway.BioImpacts : BI · 2024Article
- Targeting the apelin system for the treatment of cardiovascular diseases.Cardiovascular research · 2023Review
- Protective Role of Short-term Aerobic Exercise Against Zinc Oxide Nanoparticles-Induced Cardiac Oxidative Stress Via Possible Changes of Apelin, Angiotensin II/Angiotensin II Type I Signalling Pathway.Cardiovascular toxicology · 2023Article
- APJ as Promising Therapeutic Target of Peptide Analogues in Myocardial Infarction- and Hypertension-Induced Heart Failure.Pharmaceutics · 2023Review
- Chronic Effects of Apelin on Cardiovascular Regulation and Angiotensin II-Induced Hypertension.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Possible roles of exercise and apelin against pregnancy complications.Frontiers in endocrinology · 2022Review
- The therapeutic potential of apelin in kidney disease.Nature reviews. Nephrology · 2021Review
- Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice.BMC genomics · 2021Article
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Authors and funding
7 authors.
Funding
Abstract
Apelin is an inotropic and cardioprotective peptide that exhibits beneficial effects through activation of the APJ receptor in the pathology of cardiovascular diseases. Apelin induces the expression of angiotensin-converting enzyme 2 (ACE2) in failing hearts, thereby improving heart function in an angiotensin 1⁻7-dependent manner. Whether apelin antagonizes the over-activation of the renin⁻angiotensin system in the heart remains elusive. In this study we show that the detrimental effects of angiotensin II (Ang II) were exacerbated in the hearts of aged apelin-gene-deficient mice. Ang II-mediated cardiac dysfunction and hypertrophy were augmented in apelin knockout mice. The loss of apelin increased the ratio of angiotensin-converting enzyme (ACE) to ACE2 expression in the Ang II-stressed hearts, and Ang II-induced cardiac fibrosis was markedly enhanced in apelin knockout mice. mRNA expression of pro-fibrotic genes, such as transforming growth-factor beta (TGF-β) signaling, were significantly upregulated in apelin knockout hearts. Consistently, treatment with the ACE-inhibitor Captopril decreased cardiac contractility in apelin knockout mice. In vitro, apelin ameliorated Ang II-induced TGF-β expression in primary cardiomyocytes, accompanied with reduced hypertrophy. These results provide direct evidence that endogenous apelin plays a crucial role in suppressing Ang II-induced cardiac dysfunction and pathological remodeling.
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