ArticleJournal of cellular and molecular medicine2014
Crosstalk between AMPK activation and angiotensin II-induced hypertrophy in cardiomyocytes: the role of mitochondria.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 88 citations in OpenAlex.
- Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025Review
- Review
- Metabolic Changes in Cardiac Aging.Reviews in cardiovascular medicine · 2023Review
- Distinct Mechanisms of β-Arrestin-Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes.Drug design, development and therapy · 2023Review
- Activation of the sirtuin silent information regulator 1 pathway inhibits pathological myocardial remodeling.Frontiers in pharmacology · 2023Review
- Metformin Prevents Endothelial Dysfunction in Endometriosis through Downregulation of ET-1 and Upregulation of eNOS.Biomedicines · 2022Article
- Angiotensin II Blood Serum Levels in Piglets, after Intra-Dermal or Intra-Muscular Vaccination against PRRSV.Veterinary sciences · 2022Article
- Old and Novel Therapeutic Approaches in the Management of Hyperglycemia, an Important Risk Factor for Atherosclerosis.International journal of molecular sciences · 2022Review
- Analysis of Mitochondrial Function, Structure, and Intracellular Organization In Situ in Cardiomyocytes and Skeletal Muscles.International journal of molecular sciences · 2022Review
- Effects of Metformin in Heart Failure: From Pathophysiological Rationale to Clinical Evidence.Biomolecules · 2021Review
- The interplay between mitochondria and store-operated CaJournal of cellular and molecular medicine · 2021Review
- Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy.Biological research · 2021Article
- Analysis of Mitochondrial Calcium Retention Capacity in Cultured Cells: Permeabilized Cells Versus Isolated Mitochondria.Frontiers in physiology · 2021Article
- Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure.European heart journal · 2020Article
- Molecular, Cellular, and Clinical Evidence That Sodium-Glucose Cotransporter 2 Inhibitors Act as Neurohormonal Antagonists When Used for the Treatment of Chronic Heart Failure.Journal of the American Heart Association · 2020Review
- Anomalous AMPK-regulated angiotensin ATJournal of biomedical science · 2020Article
- Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARBioMed research international · 2020Article
- Stimulation of AlphaPPAR research · 2020Article
- C‑type natriuretic peptide prevents angiotensin II‑induced atrial connexin 40 and 43 dysregulation by activating AMP‑activated kinase signaling.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 4 countries.
Funding
Abstract
AMP-kinase (AMPK) activation reduces cardiac hypertrophy, although underlying molecular mechanisms remain unclear. In this study, we elucidated the anti-hypertrophic action of metformin, specifically, the role of the AMPK/eNOS/p53 pathway. H9c2 rat cardiomyocytes were treated with angiotensin II (AngII) for 24 hrs in the presence or absence of metformin (AMPK agonist), losartan [AngII type 1 receptor (AT1R) blocker], Nω-nitro-L-arginine methyl ester (L-NAME, pan-NOS inhibitor), splitomicin (SIRT1 inhibitor) or pifithrin-α (p53 inhibitor). Results showed that treatment with metformin significantly attenuated AngII-induced cell hypertrophy and death. Metformin attenuated AngII-induced activation (cleavage) of caspase 3, Bcl-2 down-regulation and p53 up-regulation. It also reduced AngII-induced AT1R up-regulation by 30% (P < 0.05) and enhanced AMPK phosphorylation by 99% (P < 0.01) and P-eNOS levels by 3.3-fold (P < 0.01). Likewise, losartan reduced AT1R up-regulation and enhanced AMPK phosphorylation by 54% (P < 0.05). The AMPK inhibitor, compound C, prevented AT1R down-regulation, indicating that metformin mediated its effects via AMPK activation. Beneficial effects of metformin and losartan converged on mitochondria that demonstrated high membrane potential (Δψm ) and low permeability transition pore opening. Thus, this study demonstrates that the anti-hypertrophic effects of metformin are associated with AMPK-induced AT1R down-regulation and prevention of mitochondrial dysfunction through the SIRT1/eNOS/p53 pathway.
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Registered trials
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.