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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Cell Mol Life Sci. 2016 Jun 6;73(22):4175–4202. doi: 10.1007/s00018-016-2285-z

Fig. 2. Endogenous and exogenous repair of striated muscles.

Fig. 2

A) Damage to skeletal muscle results in proliferation and migration of satellite cells (SCs) along the longitudinal axis of dying fibers (gray) and initial infiltration of pro-inflammatory M1-macrophages and neutrophils which aids in the degeneration of damaged fibers. Conversion to and infiltration of M2-macrophages stimulates SCs to differentiate and eventually fuse into functional myofibers. B) Ischemic injury to cardiac muscle results in death of cardiomyocytes (CMs), an initial infiltration of neutrophils and upregulation of matrix metalloproteinases. Release of TGF-β from necrotic CMs induces late migration of macrophages and fibroblasts as well as transformation of fibroblasts into myofibroblasts, which secrete collagen to ultimately produce a fibrotic scar. C) Striated muscle repair can be augmented via exogenous delivery of single cells, biomaterials with or without cells, as well as transplantation of in vitro engineered functional muscle tissues.