Abstract
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.
Highlights
Pathological inflammation, a hallmark of numerous chronic diseases, can lead to fatal comorbidities, including cachexia [1,2,3,4]
No treatments are currently approved for cancer cachexia, improving the mechanistic understanding of skeletal muscle mass loss and more recently skeletal muscle metabolic function is thought to be central to the etiology of cancer cachexia and the successful development of therapeutic interventions
Dysfunctional muscle oxidative metabolism occurs with many disease conditions [12, 13, 18,19,20,21] and can involve mitochondrial dynamics, mitophagy, and biogenesis regulation [18, 22]
Summary
Pathological inflammation, a hallmark of numerous chronic diseases, can lead to fatal comorbidities, including cachexia [1,2,3,4]. Dysfunctional muscle oxidative metabolism occurs with many disease conditions [12, 13, 18,19,20,21] and can involve mitochondrial dynamics, mitophagy, and biogenesis regulation [18, 22] Each of these dysfunctions is being actively investigated for their role in the pathogenesis of cancer cachexia [12, 13, 23]. The examination of inflammatory mediators of cancer cachexia will be delimited to interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and transforming growth factor β (TGF-β) superfamilies’ role Evidence for these cytokines in the overall regulation of cachexia progression and muscle mass loss has been extensively reviewed elsewhere [29,30,31,32,33,34,35,36,37,38] and will only be briefly described here. We will discuss the potential for either muscle inactivity or exercise to alter the regulation of dysfunctional mitochondrial dynamics, mitophagy, and biogenesis during cancer cachexia
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