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- W2211849424 abstract "Pathologic fibrosis in the aging mouse heart is associated with dysregulated resident mesenchymal stem cells (MSC) arising from reduced stemness and aberrant differentiation into dysfunctional inflammatory fibroblasts. Fibroblasts derived from aging MSC secrete higher levels of 1) collagen type 1 (Col1) that directly contributes to fibrosis, 2) monocyte chemoattractant protein-1 (MCP-1) that attracts leukocytes from the blood and 3) interleukin-6 (IL-6) that facilitates transition of monocytes into myeloid fibroblasts. The transcriptional activation of these proteins is controlled via the farnesyltransferase (FTase)-Ras-Erk pathway. The intrinsic change in the MSC phenotype acquired by advanced age is specific for the heart since MSC originating from bone wall (BW-MSC) or fibroblasts derived from them were free of these defects. The potential therapeutic interventions other than clinically approved strategies based on findings presented in this review are discussed as well. This article is a part of a Special Issue entitled Fibrosis and Myocardial Remodeling." @default.
- W2211849424 created "2016-06-24" @default.
- W2211849424 creator A5046577754 @default.
- W2211849424 creator A5052376231 @default.
- W2211849424 creator A5063913292 @default.
- W2211849424 date "2016-02-01" @default.
- W2211849424 modified "2023-10-06" @default.
- W2211849424 title "Mesenchymal stem cell-derived inflammatory fibroblasts mediate interstitial fibrosis in the aging heart" @default.
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- W2211849424 doi "https://doi.org/10.1016/j.yjmcc.2015.12.017" @default.
- W2211849424 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4764495" @default.