Journal
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
Volume 99, Issue -, Pages 109-113Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2018.04.002
Keywords
Perivascular cells; Skeletal muscle; Fibrosis; Integrins; PDGFR beta
Categories
Funding
- Instituto Serrapilheira [G-1708-15285]
- Pro-reitoria de Pesquisa/Universidade Federal de Minas Gerais (PRPq/UFMG)
- FAPEMIG [Rede Mineira de Engenharia de Tecidos e Terapia Celular (REMETTEC)] [RED-00570-16]
- FAPEMIG [Rede De Pesquisa Em Doencas Infecciosas Humanas E Animais Do Estado De Minas Gerais] [RED-00313-16]
- National Institutes of Health (NIH) [1R01CA179072-01A1]
- American Cancer Society Mentored Research Scholar grant [124443-MRSG-13-121-01-CDD]
- NIH [R01AG013934, R01AG057013]
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Fibrosis following injury leads to aberrant regeneration and incomplete functional recovery of skeletal muscle, but the lack of detailed knowledge about the cellular and molecular mechanisms involved hampers the design of effective treatments. Using state-of-the-art technologies, Murray et al. (2017) found that perivascular PDGFR beta-expressing cells generate fibrotic cells in the skeletal muscle. Strikingly, genetic deletion of alpha v integrins from perivascular PDGFR beta-expressing cells significantly inhibited skeletal muscle fibrosis without affecting muscle vascularization or regeneration. In addition, the authors showed that a small molecule inhibitor of alpha v integrins, CWHM 12, attenuates skeletal muscle fibrosis. From a drug-development perspective, this study identifies a new cellular and molecular target to treat skeletal muscle fibrosis.
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