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1.
Nat Commun ; 12(1): 692, 2021 01 29.
Article in English | MEDLINE | ID: mdl-33514709

ABSTRACT

Skeletal muscle has remarkable regeneration capabilities, mainly due to its resident muscle stem cells (MuSCs). In this review, we introduce recently developed technologies and the mechanistic insights they provide to the understanding of MuSC biology, including the re-definition of quiescence and Galert states. Additionally, we present recent studies that link MuSC function with cellular heterogeneity, highlighting the complex regulation of self-renewal in regeneration, muscle disorders and aging. Finally, we discuss MuSC metabolism and its role, as well as the multifaceted regulation of MuSCs by their niche. The presented conceptual advances in the MuSC field impact on our general understanding of stem cells and their therapeutic use in regenerative medicine.


Subject(s)
Muscle, Skeletal/cytology , Muscular Diseases/therapy , Regenerative Medicine/methods , Stem Cell Transplantation/methods , Stem Cells/physiology , Animals , Disease Models, Animal , Humans , Muscle, Skeletal/physiology , Muscular Diseases/physiopathology , Regeneration/physiology
2.
J Physiol ; 591(23): 6017-37, 2013 Dec 01.
Article in English | MEDLINE | ID: mdl-24042504

ABSTRACT

The role of OPA1, a GTPase dynamin protein mainly involved in the fusion of inner mitochondrial membranes, has been studied in many cell types, but only a few studies have been conducted on adult differentiated tissues such as cardiac or skeletal muscle cells. Yet OPA1 is highly expressed in these cells, and could play different roles, especially in response to an environmental stress like exercise. Endurance exercise increases energy demand in skeletal muscle and repeated activity induces mitochondrial biogenesis and activation of fusion-fission cycles for the synthesis of new mitochondria. But currently no study has clearly shown a link between mitochondrial dynamics and biogenesis. Using a mouse model of haploinsufficiency for the Opa1 gene (Opa1(+/-)), we therefore studied the impact of OPA1 deficiency on the adaptation ability of fast skeletal muscles to endurance exercise training. Our results show that, surprisingly, Opa1(+/-) mice were able to perform the same physical activity as control mice. However, the adaptation strategies of both strains after training differed: while in control mice mitochondrial biogenesis was increased as expected, in Opa1(+/-) mice this process was blunted. Instead, training in Opa1(+/-) mice led to an increase in endurance capacity, and a specific adaptive response involving a metabolic remodelling towards enhanced fatty acid utilization. In conclusion, OPA1 appears necessary for the normal adaptive response and mitochondrial biogenesis of skeletal muscle to training. This work opens new perspectives on the role of mitochondrial dynamics in skeletal muscle cells and during adaptation to stress.


Subject(s)
GTP Phosphohydrolases/physiology , Mitochondria, Muscle/physiology , Muscle, Skeletal/physiology , Physical Conditioning, Animal/physiology , Physical Endurance/physiology , Animals , Behavior, Animal/physiology , DNA/metabolism , Male , Mice , Mice, Knockout , Microscopy, Electron , Mitochondria, Muscle/ultrastructure , Psychomotor Performance/physiology , Running
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