Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Nov;23(6):568-73.
doi: 10.1097/BOR.0b013e32834bac92.

Regeneration versus fibrosis in skeletal muscle

Affiliations
Review

Regeneration versus fibrosis in skeletal muscle

Adam L Moyer et al. Curr Opin Rheumatol. 2011 Nov.

Abstract

Purpose of review: This review evaluates recently published literature examining various muscle tissue cells and their modulators that determine whether injured skeletal muscle will fully regenerate or become fibrotic.

Recent findings: Muscle regeneration is a complex process involving several interacting cell types. Macrophages initiate a cytokine response to injury that both directs the subsequent inflammatory response and promotes nonmyeloid proliferation. Muscle cells and their progenitors produce autocrine and paracrine growth factors that help inhibit or stimulate muscle growth and regeneration. Cells of the connective tissue, including fibroblasts and newly described fibro/adipogenic progenitors, can support myogenic cells and remodel the extracellular matrix. However in certain environments, fibrosis can become a self-perpetuating process leading to incomplete muscle regeneration.

Summary: Several cell types are involved in the muscle repair process, interacting through multiple signaling molecules and pathways. This provides a richness of potential therapeutic targets to reduce fibrosis and facilitate skeletal muscle regeneration.

PubMed Disclaimer

Similar articles

Cited by

Publication types

LinkOut - more resources