ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Adiponectin mediates cardioprotection in oxidative stress-induced cardiac myocyte remodeling.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 109 citations in OpenAlex.
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- ATGL From iWAT and BAT Is Crucial for Cardiac Remodeling and Metabolism After Myocardial Ischemia/Reperfusion.Comprehensive Physiology · 2026Article
- Molecular insights in HIV-associated cardiac dysfunction.Communications medicine · 2025Article
- Review
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Downregulation of PGAM2 alleviates angiotensin II-induced cardiac hypertrophy by destabilizing HSP90 and inactivating the mTOR/IKKα signaling pathway.International journal of biological sciences · 2025Article
- The change of epicardial adipose tissue characteristics and vulnerability for atrial fibrillation upon drastic weight loss.Adipocyte · 2024Article
- Prediction of cardiac death in patients with hypertrophic cardiomyopathy using plasma adipokine levels.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2024Article
- The role of oxidative stress in aortic dissection: a potential therapeutic target.Frontiers in cardiovascular medicine · 2024Review
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Adiponectin and metabolic cardiovascular diseases: Therapeutic opportunities and challenges.Genes & diseases · 2023Review
- Short-Chain Fatty Acids in Gut-Heart Axis: Their Role in the Pathology of Heart Failure.Journal of personalized medicine · 2022Review
- Contraction Band Necrosis with Dephosphorylated Connexin 43 in Rat Myocardium after Daily Cocaine Administration.International journal of molecular sciences · 2022Article
- Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis.American journal of physiology. Heart and circulatory physiology · 2022Article
- Adiponectin accumulation in the retinal vascular endothelium and its possible role in preventing early diabetic microvascular damage.Scientific reports · 2022Article
- Role of adiponectin in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications.Physiological reviews · 2021Review
- Galangin Resolves Cardiometabolic Disorders through Modulation of AdipoR1, COX-2, and NF-κB Expression in Rats Fed a High-Fat Diet.Antioxidants (Basel, Switzerland) · 2021Article
- Heal the heart through gut (hormone) ghrelin: a potential player to combat heart failure.Heart failure reviews · 2021Review
- Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
Reactive oxygen species (ROS) induce matrix metalloproteinase (MMP) activity that mediates hypertrophy and cardiac remodeling. Adiponectin (APN), an adipokine, modulates cardiac hypertrophy, but it is unknown if APN inhibits ROS-induced cardiomyocyte remodeling. We tested the hypothesis that APN ameliorates ROS-induced cardiomyocyte remodeling and investigated the mechanisms involved. Cultured adult rat ventricular myocytes (ARVM) were pretreated with recombinant APN (30 μg/ml, 18 h) followed by exposure to physiologic concentrations of H(2)O(2) (1-200 μM). ARVM hypertrophy was measured by [(3)H]leucine incorporation and atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) gene expression by RT-PCR. MMP activity was assessed by in-gel zymography. ROS was induced with angiotensin (ANG)-II (3.2 mg·kg(-1)·day(-1) for 14 days) in wild-type (WT) and APN-deficient (APN-KO) mice. Myocardial MMPs, tissue inhibitors of MMPs (TIMPs), p-AMPK, and p-ERK protein expression were determined. APN significantly decreased H(2)O(2)-induced cardiomyocyte hypertrophy by decreasing total protein, protein synthesis, ANF, and BNP expression. H(2)O(2)-induced MMP-9 and MMP-2 activities were also significantly diminished by APN. APN significantly increased p-AMPK in both nonstimulated and H(2)O(2)-treated ARVM. H(2)O(2)-induced p-ERK activity and NF-κB activity were both abrogated by APN pretreatment. ANG II significantly decreased myocardial p-AMPK and increased p-ERK expression in vivo in APN-KO vs. WT mice. ANG II infusion enhanced cardiac fibrosis and MMP-2-to-TIMP-2 and MMP-9-to-TIMP-1 ratios in APN-KO vs. WT mice. Thus APN inhibits ROS-induced cardiomyocyte remodeling by activating AMPK and inhibiting ERK signaling and NF-κB activity. Its effects on ROS and ultimately on MMP expression define the protective role of APN against ROS-induced cardiac remodeling.
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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.