AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction
Katarzyna A. Cieslik; George E. Taffet; Jeffrey R. Crawford; JoAnn Trial; Patricia Mejia Osuna; Mark L. Entman · 2013 · Journal of Molecular and Cellular Cardiology
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
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)
Abstract by Katarzyna A. Cieslik; George E. Taffet; Jeffrey R. Crawford; JoAnn Trial; Patricia Mejia Osuna; Mark L. Entman, Journal of Molecular and Cellular Cardiology (2013) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1016/j.yjmcc.2013.07.005