4.3 Review

Mitochondrial Dysfunction in Skeletal Muscle Pathologies

Journal

CURRENT PROTEIN & PEPTIDE SCIENCE
Volume 20, Issue 6, Pages 536-546

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389203720666190402100902

Keywords

Mitochondria; ROS; skeletal muscle; atrophy; dystrophy; ATP production

Funding

  1. National Fund for Science & Technology Development [FONDECYT 1161646, 1161288, 1161438, 11171001]
  2. Millennium Institute on Immunology and Immunotherapy [P09-016-F]
  3. Programa de Cooperacion Cientifica ECOS-CONICYT [C16S02]
  4. Center for Aging and Regeneration [CARE PFB12/2007]
  5. BASAL Grant CEDENNA [FB0807]
  6. H2020-MSCA-RISE-2016 [734801 MAG-NAMED]
  7. Nucleus-UNAB [DI 36-18/N]
  8. Conicyt [21161353]

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Several molecular mechanisms are involved in the regulation of skeletal Muscle function. Among them, mitochondrial activity can be identified. The mitochondria is an important and essential organelle in the skeletal muscle that is involved in metabolic regulation and ATP production, which are two key elements of muscle contractibility and plasticity. Thus, in this review, we present the critical and recent antecedents regarding the mechanisms through which mitochondrial dysfunction can be involved in the generation and development of skeletal muscle pathologies, its contribution to detrimental functioning in skeletal muscle and its crosstalk with other typical signaling pathways related to muscle diseases. In addition, an update on the development of new strategies with therapeutic potential to inhibit the deleterious impact of mitochondrial dysfunction in skeletal muscle is discussed.

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