Copyright
©2014 Baishideng Publishing Group Inc.
World J Cardiol. Jul 26, 2014; 6(7): 610-620
Published online Jul 26, 2014. doi: 10.4330/wjc.v6.i7.610
Published online Jul 26, 2014. doi: 10.4330/wjc.v6.i7.610
Factor | Outcome | Ref. |
↑Akt | Reduction cardiomyocyte loss | [52] |
↓ NF-κβ | Anti-apoptotic effects | [53-55] |
↓ TNF-α | Anti-apoptotic effects | [53-55] |
↓ IL-6 | Anti-apoptotic effects | [53-55] |
↑ IL-10 | Anti-apoptotic effects | [53-55] |
↑ IL-6 | Prevention activated neutrophil apoptosis via Stat3; regulation of neutrophil activation | [56-60] |
↑ IL-10, ↑TNF-α, and ↑ IL-6 | Macrophage M2 polarization | [53,61-65] |
↓ Collagen I and III, ↓ TIMP-1 and ↓TGF-β | Reduction in fibrosis and scar size | [55,69-76] |
↑ VEGF | Promote angiogenesis; improved contractile function | [77-86] |
↑ IL-6 | DC maturation inhibition | [60,66-68] |
↑ IDO and ↑PGE2 | Reduced T cell activation | [60,66-68] |
↑ IDO and ↑PGE2 | Decreased NK proliferation | [60] |
Factor to be identified | B-Cell arrest | [60] |
- Citation: Zamilpa R, Navarro MM, Flores I, Griffey S. Stem cell mechanisms during left ventricular remodeling post-myocardial infarction: Repair and regeneration. World J Cardiol 2014; 6(7): 610-620
- URL: https://www.wjgnet.com/1949-8462/full/v6/i7/610.htm
- DOI: https://dx.doi.org/10.4330/wjc.v6.i7.610