Macrophages Fuel Skeletal Muscle Regeneration.

Joel D Schilling

doi:10.20900/immunometab20210013

Abstract

In this commentary we discuss new findings presented by Shang et al. regarding the role of macrophage-derived glutamine in skeletal muscle repair. Loss-of-function of glutamate dehydrogenase in macrophages led to an upregulation of glutamine synthesis which sustained glutamine levels in muscle tissue and facilitated satellite cell proliferation and differentiation.

Highlights

Macrophages are cells of the innate immune system that play a critical role in the regulation of inflammatory responses
Tissue resident macrophages contribute to organ development and homeostasis, whereas monocyte-derived macrophages are recruited upon tissue injury and coordinate tissue inflammation and repair
As GLUD1 catalyzes the conversion of glutamate to α-ketoglutarate for entry into the tricarboxylic acid (TCA) cycle it was not surprising that KO macrophages had a ~75% reduction in glutamine oxidation capacity

Summary

Introduction

Macrophages are cells of the innate immune system that play a critical role in the regulation of inflammatory responses. Macrophages contribute to skeletal muscle regeneration via several mechanisms including the release of cytokines that promote repair, such as IL-6 and TGFβ, and growth factors, including IGF-1, that can stimulate expansion of the muscle stem cells [6,7,8]. In an elegant recent study, Shang et al investigate the role of metabolites as mediators of crosstalk between macrophages and muscle satellite cells, an area which had not previously been explored. The authors describe a novel mechanism linking macrophage glutamine metabolism to muscle repair [9].

Results

Conclusion