| Literature DB >> 28365093 |
Yonggang Ma1, Rugmani Padmanabhan Iyer1, Mira Jung1, Michael P Czubryt2, Merry L Lindsey3.
Abstract
In response to myocardial infarction (MI), the wound healing response of the left ventricle (LV) comprises overlapping inflammatory, proliferative, and maturation phases, and the cardiac fibroblast is a key cell type involved in each phase. It has recently been appreciated that, early post-MI, fibroblasts transform to a proinflammatory phenotype and secrete cytokines and chemokines as well as matrix metalloproteinases (MMPs). Later post-MI, fibroblasts are activated to anti-inflammatory and proreparative phenotypes and generate anti-inflammatory and proangiogenic factors and extracellular matrix (ECM) components that form the infarct scar. Additional studies are needed to systematically examine how fibroblast activation shifts over the timeframe of the MI response and how modulation at different activation stages could alter wound healing and LV remodeling in distinct ways. This review summarizes current fibroblast knowledge as the foundation for a discussion of existing knowledge gaps.Entities:
Keywords: big data; computational models; extracellular matrix; fibroblast; inflammation; myocardial infarction; omics
Mesh:
Year: 2017 PMID: 28365093 PMCID: PMC5437868 DOI: 10.1016/j.tips.2017.03.001
Source DB: PubMed Journal: Trends Pharmacol Sci ISSN: 0165-6147 Impact factor: 14.819