Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation.
Brandon N VanderVeenDennis K FixJames A CarsonPublished in: Oxidative medicine and cellular longevity (2017)
Chronic inflammation is a hallmark of cancer cachexia in both patients and preclinical models. Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulation of cancer cachexia. An established characteristic of cachectic skeletal muscle is a disrupted capacity for oxidative metabolism, which is thought to contribute to cancer patient fatigue, diminished metabolic function, and muscle mass loss. This review's primary objective is to highlight emerging evidence linking cancer-induced inflammation to the dysfunctional regulation of mitochondrial dynamics, mitophagy, and biogenesis in cachectic muscle. The potential for either muscle inactivity or exercise to alter mitochondrial dysfunction during cancer cachexia will also be discussed.
Keyphrases
- papillary thyroid
- skeletal muscle
- oxidative stress
- squamous cell
- adipose tissue
- stem cells
- end stage renal disease
- squamous cell carcinoma
- chronic kidney disease
- metabolic syndrome
- childhood cancer
- mesenchymal stem cells
- epithelial mesenchymal transition
- body composition
- newly diagnosed
- transforming growth factor
- climate change
- cell therapy
- drug induced