ArticleThe American journal of pathology2011
Defective myofibroblast formation from mesenchymal stem cells in the aging murine heart rescue by activation of the AMPK pathway.
Article in The American journal of pathology, 2011. 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, 56 citations in OpenAlex.
- Myosin light chain kinase 2 and Myomesin 2 are related to the stiffness of vocal fold lamina propria in aging rats and humans.Biogerontology · 2025Article
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- Aging-associated mechanisms of atrial fibrillation progression and their therapeutic potential.The journal of cardiovascular aging · 2024Article
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Article
- Therapeutic opportunities for senolysis in cardiovascular disease.The FEBS journal · 2023Review
- Transplanted allogeneic cardiac progenitor cells secrete GDF-15 and stimulate an active immune remodeling process in the ischemic myocardium.Journal of translational medicine · 2022Article
- Treatment with a DC-SIGN ligand reduces macrophage polarization and diastolic dysfunction in the aging female but not male mouse hearts.GeroScience · 2021Article
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
- 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
- Differential Gender-Dependent Patterns of Cardiac Fibrosis and Fibroblast Phenotypes in Aging Mice.Oxidative medicine and cellular longevity · 2020Article
- Modelling cardiac fibrosis using three-dimensional cardiac microtissues derived from human embryonic stem cells.Journal of biological engineering · 2019Article
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
- Aicar treatment reduces interstitial fibrosis in aging mice: Suppression of the inflammatory fibroblast.Journal of molecular and cellular cardiology · 2017Article
- Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis.Basic research in cardiology · 2017Article
- Knockdown of Plakophilin 2 Downregulates miR-184 Through CpG Hypermethylation and Suppression of the E2F1 Pathway and Leads to Enhanced Adipogenesis In Vitro.Circulation research · 2016Article
- Mesenchymal stem cell-derived inflammatory fibroblasts mediate interstitial fibrosis in the aging heart.Journal of molecular and cellular cardiology · 2016Review
- Ghrelin Inhibits Post-Operative Adhesions via Blockage of the TGF-β Signaling Pathway.PloS one · 2016Article
- Mesenchymal stem cell-derived inflammatory fibroblasts promote monocyte transition into myeloid fibroblasts via an IL-6-dependent mechanism in the aging mouse heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Aged mice in a murine model of myocardial infarction exhibit less effective myocardial repair. We hypothesized that the deficiency arises from altered lineage choice of endogenous mesenchymal stem cells (MSCs) and faulty maturation of myofibroblasts. Examination of cardiac MSCs revealed a substantial reduction in the pluripotency marker Nanog in cells from aged mice. In addition, the aged MSCs demonstrated a redirected lineage choice that favored adipocytic commitment over fibroblast or myofibroblast differentiation. Fibroblasts derived from aged MSCs demonstrated reduced expression of transforming growth factor-β (TGF-β) receptors I and II and diminished SMAD3 phosphorylation, associated with attenuated contractility and migration. Overexpression of constitutively active TGF-β receptor I in aged cardiac fibroblasts ameliorated their defective motility but did not improve their contractility. Culturing of MSCs and fibroblasts with AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside) to activate adenosine monophosphate-activated kinase resulted in TGF-β-dependent development of myofibroblasts with markedly enhanced contractility despite no reduction in adipocytic commitment or increased expression of TGF-β receptors and SMAD3 phosphorylation. The data suggest an adenosine monophosphate-activated kinase-dependent gain of function as mediated by phosphorylation of TGF-β-activated kinase 1 and p38 mitogen-activated protein kinase, which amplifies the response to TGF-β1 via a non-canonical pathway, thus compensating for the reduced expression of TGF-β receptors.
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Registered trials
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