PuSH - Publikationsserver des Helmholtz Zentrums München

Schiaffino, S.* ; Dyar, K.A. ; Calabria, E.*

Skeletal muscle mass is controlled by the MRF4-MEF2 axis.

Curr. Opin. Clin. Nutr. Metab. Care 21, 164-167 (2018)
Verlagsversion DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Purpose of reviewThe review is focused on the unexpected role of myogenic regulatory factor 4 (MRF4) in controlling muscle mass by repressing myocyte enhancer binding factor 2 (MEF2) activity in adult skeletal muscle, and on the emerging role of MEF2 in skeletal muscle growth.Recent findingsThe MRF4s of the MyoD family (MyoD, MYF5, MRF4, myogenin) and the MEF2 factors are known to play a major role in embryonic myogenesis. However, their function in adult muscle tissue is not known. A recent study shows that MRF4 loss in adult skeletal muscle causes muscle hypertrophy and prevents denervation atrophy. This effect is mediated by MEF2 factors that promote muscle growth, with MRF4 acting as a repressor of MEF2 activity. The role of MEF2 in skeletal muscle growth is supported by the finding that muscle regeneration is impaired by muscle-specific triple knockout of Mef2a, c, and d genes.SummaryThe finding that the MRF4-MEF2 axis controls muscle growth opens a new perspective for preventing muscle wasting. A unique feature of this pathway is that MRF4 is exclusively expressed in skeletal muscle, thus reducing the risk that interventions aimed at down-regulating MRF4 or interfering with the interaction between MRF4 and MEF2 may have off-target effects in other tissues.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Myocyte Enhancer Binding Factor 2 ; Myogenic Regulatory Factor 4 ; Muscle Atrophy ; Muscle Hypertrophy ; Skeletal Muscle; Hypertrophy; Mef2; Differentiation; Regeneration; Myogenesis; Growth; Cells; Mrf4
ISSN (print) / ISBN 1363-1950
e-ISSN 1473-6519
Zeitschrift Current Opinion in Clinical Nutrition & Metabolic Care
Quellenangaben Band: 21, Heft: 3, Seiten: 164-167 Artikelnummer: , Supplement: ,
Verlag Lippincott Williams & Wilkins
Verlagsort Philadelphia
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)