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Loss of HDAC11 accelerates skeletal muscle regeneration in mice
Author(s) -
NúñezÁlvarez Yaiza,
Hurtado Erica,
Muñoz Mar,
GarcíaTuñon Ignacio,
Rech Gabriel E.,
Pluvinet Raquel,
Sumoy Lauro,
Pendás Alberto M.,
Peinado Miguel A.,
Suelves Mònica
Publication year - 2021
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.15468
Subject(s) - biology , skeletal muscle , regeneration (biology) , hdac11 , histone deacetylase , microbiology and biotechnology , stem cell , population , immunology , cancer research , histone , genetics , endocrinology , medicine , gene , environmental health
Upon acute muscle damage, HDAC11 is involved in regeneration processes, both satellite and inflammatory cell‐dependent. HDAC11‐deficient myoblasts proliferate longer and present a delayed cell cycle exit, with sustained expression of proliferation genes at early differentiation. Differentiating HDAC11 −/− myocytes express higher levels of myogenin, and regenerating myofibers show an increased size. Recruited macrophages secrete increased M1 pro‐inflammatory and M2 anti‐inflammatory cytokines that further enhance HDAC11 KO muscle regeneration capacity.