ArticleJournal of molecular and cellular cardiology2013
AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 58 citations in OpenAlex.
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- Purine Nucleotide Precursors in Preventing Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Cardioprotective effects of AMPK activation in H1N1 influenza virus infection.bioRxiv : the preprint server for biology · 2025Article
- Metformin lotion as a novel approach to prevent tendinopathy induced by mechanical overuse.Scientific reports · 2025Article
- AMP-dependent kinase stimulates the expression of αKlotho.FEBS open bio · 2024Article
- AMPK, a key molecule regulating aging-related myocardial ischemia-reperfusion injury.Molecular biology reports · 2024Review
- Metformin lotion promotes scarless skin tissue formation through AMPK activation, TGF-β1 inhibition, and reduced myofibroblast numbers.PloS one · 2024Article
- Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges.Nature reviews. Cardiology · 2023Review
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- Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis.American journal of physiology. Heart and circulatory physiology · 2022Article
- Sex matters in the aging heart: implications for antifibrotic therapies.American journal of physiology. Heart and circulatory physiology · 2022Article
- The Potential of Gamma Secretase as a Therapeutic Target for Cardiac Diseases.Journal of personalized medicine · 2021Review
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- Emodin induces collagen type I synthesis in Hs27 human dermal fibroblasts.Experimental and therapeutic medicine · 2021Article
- AdipoRon Attenuates Inflammation and Impairment of Cardiac Function Associated With Cardiopulmonary Bypass-Induced Systemic Inflammatory Response Syndrome.Journal of the American Heart Association · 2021Article
- Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse.Scientific reports · 2021Article
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
- Cardiomyocyte Senescence and Cellular Communications Within Myocardial Microenvironments.Frontiers in endocrinology · 2020Review
- Transient activation of AMPK preceding left ventricular pressure overload reduces adverse remodeling and preserves left ventricular function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- AdipoRon, an adiponectin receptor agonist, attenuates cardiac remodeling induced by pressure overload.Journal of molecular medicine (Berlin, Germany) · 2018Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We have demonstrated that scar formation after myocardial infarction (MI) is associated with an endogenous pool of CD44(pos)CD45(neg) multipotential mesenchymal stem cells (MSC). MSC differentiate into fibroblasts secreting collagen that forms a scar and mature into myofibroblasts that express alpha smooth muscle actin (α-SMA) that stabilizes the scar. In the aging mouse, cardiac repair after MI is associated with impaired differentiation of MSC; MSC derived from the aged hearts form dysfunctional fibroblasts that deposit less collagen in response to transforming growth factor beta-1 (TGF-β1) and poorly mature into myofibroblasts. We found in vitro that the defect in myofibroblast maturation can be remedied by AICAR, which activates non-canonical TGF-β signaling through AMP-activated protein kinase (AMPK). In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days. AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct. This was accompanied by enhanced collagen deposition and collagen fiber maturation in the scar. The AICAR-treated group has demonstrated reduced adverse remodeling as indicated by improved apical end diastolic dimension but no changes in ejection fraction and cardiac output were observed. We concluded that these data indicate the novel, previously not described role of AMPK in the post-MI scar formation. These findings can potentially lead to a new therapeutic strategy for prevention of adverse remodeling in the aging heart.
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