4.7 Review

Cardiac Fibroblast Activation Post-Myocardial Infarction: Current Knowledge Gaps

Journal

TRENDS IN PHARMACOLOGICAL SCIENCES
Volume 38, Issue 5, Pages 448-458

Publisher

ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tips.2017.03.001

Keywords

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Funding

  1. American Heart Association [15SDG22930009]
  2. Canadian Institutes of Health Research [MOP-136862]
  3. National Heart, Lung, and Blood Institute
  4. National Institute of General Medical Sciences of the National Institutes of Health [HL075360, HL129823, HL051971, GM104357, GM114833, GM115428]
  5. Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [5I01BX000505]

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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.

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