Reviews
Mitochondrial transfer and implications for muscle function in idiopathic inflammatory myopathies
J.A. Gonzalez Chapa1, M. Barguil Macêdo2, E. Naddaf3, L.A. Saketkoo4, C. Lood5
- Division of Rheumatology, University of Washington, Seattle, WA, USA.
- Division of Rheumatology, University of Washington, Seattle, WA, USA.
- Department of Neurology, Mayo Clinic, Rochester, MN, USA.
- Department of Medicine, Lousiana State University and Tulane University Schools of Medicine, New Orleans, LA, USA.
- Division of Rheumatology, University of Washington, Seattle, WA, USA. loodc@uw.edu
for the International Myositis Health and Research Collaborative Alliance (MIHRA) Mitochondria Scientific Working Group
CER17201
2024 Vol.42, N°2
PI 0394, PF 0402
Reviews
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PMID: 38293948 [PubMed]
Received: 15/10/2023
Accepted : 11/12/2023
In Press: 25/01/2024
Published: 14/03/2024
Abstract
Impairment in cellular bioenergetics as either the cause, consequence, or major contributor of tissue damage has drawn increasing scientific curiosity across aging and chronic health conditions, with mitochondrial dysfunction emerging as a central mechanism in the pathogenesis of a variety of inflammatory and degenerative disorders. Beyond bioenergetics, mitochondria play critical regulatory roles in programmed cell death of dysfunctional/defective cells as well as in metabolite synthesis and metabolic signalling. Further, extra-cellular exposure to fragmentation of injured mitochondria is associated with incitement of systemic and organ-based inflammation. Thus, mitochondrial function has recently drawn intense, spectral scientific interest as an integral component across maladies. In muscle, mitochondrial dysfunction is clinically associated with atrophy and diminished endurance. Direct myo-histopathological evidence characterising loss of mitochondrial integrity as a hallmark of muscle compromise was first noticed in inclusion body myositis (IBM). This was followed by the discovery of multiple deletions in mitochondrial DNA in sarcopenia, IBM, and other inflammatory myopathies, like dermatomyositis. Though fraught with bioethical considerations, the transplant technology of mitochondrial transfer is swiftly gaining prominence in cellular biology and muscle physiology to remediate mitochondrial diminution and dysfunction. Assembling seminal works and recent developments, this review ventures into the rapidly evolving landscape of mitochondrial transfer, focusing on its implications on muscle function, and offers an integrated perspective on the potential roles of mitochondrial transfer and its implications for preserving and restoring muscle health. Presented here is a consolidated viewpoint on mitochondrial transfer in idiopathic inflammatory myopathies.
