| المؤلفون: |
Sligar J; Mitochondrial Metabolism and Ageing Laboratory, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.; St Vincent's Medical School, UNSW Medicine, UNSW Sydney, Sydney, New South Wales, Australia., DeBruin DA; Australian Institute for Musculoskeletal Science, Victoria University, Sunshine Hospital, St Albans, Victoria, Australia.; Institute for Health and Sport, Victoria University, Melbourne, Victoria, Australia., Saner NJ; Human Integrative Physiology, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Philp AM; Mitochondrial Metabolism and Ageing Laboratory, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.; St Vincent's Medical School, UNSW Medicine, UNSW Sydney, Sydney, New South Wales, Australia., Philp A; Mitochondrial Metabolism and Ageing Laboratory, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.; St Vincent's Medical School, UNSW Medicine, UNSW Sydney, Sydney, New South Wales, Australia. |
| مستخلص: |
As the principal energy-producing organelles of the cell, mitochondria support numerous biological processes related to metabolism, growth, and regeneration in skeletal muscle. Deterioration in skeletal muscle functional capacity with age is thought to be driven in part by a reduction in skeletal muscle oxidative capacity and reduced fatigue resistance. Underlying this maladaptive response is the development of mitochondrial dysfunction caused by alterations in mitochondrial quality control (MQC), a term encompassing processes of mitochondrial synthesis (biogenesis), remodeling (dynamics), and degradation (mitophagy). Knowledge regarding the role and regulation of MQC in skeletal muscle and the influence of aging in this process has rapidly advanced in the past decade. Given the emerging link between aging and MQC, therapeutic approaches to manipulate MQC to prevent mitochondrial dysfunction during aging hold tremendous therapeutic potential. |
