Oxidative stress: Roles in skeletal muscle atrophy

Zhang, Han; Qi, Guangdong; Wang, Kexin; Yang, Junru; Shen, Yuntian; Xiaoming, Yang; Chen, Xin; Yao, Xin; Gu, Xiaosong; Qi, Lei; Zhang, Chun; Sun, Hualin

doi:10.1016/j.bcp.2023.115664

Cited by 63 publications

(18 citation statements)

References 176 publications

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“…Moreover, cancer cell-derived EVs interfere with muscle regeneration by affecting the activation and differentiation of muscle cells [ 57 ]. These EVs can transport bioactive molecules like oxidized proteins, which, when internalized by muscle cells, disrupt the cellular redox balance, leading to oxidative stress and the degradation of contractile proteins [ 47 , 78 ]. Furthermore, cancer cell-derived EVs may influence the contractile properties of muscle cells.…”

Section: Evs and Pathogenesis Of CCmentioning

confidence: 99%

Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons

Wang,

Ding

2024

J Transl Med

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Cancer cachexia (CC) is a debilitating syndrome that affects 50–80% of cancer patients, varying in incidence by cancer type and significantly diminishing their quality of life. This multifactorial syndrome is characterized by muscle and fat loss, systemic inflammation, and metabolic imbalance. Extracellular vesicles (EVs), including exosomes and microvesicles, play a crucial role in the progression of CC. These vesicles, produced by cancer cells and others within the tumor environment, facilitate intercellular communication by transferring proteins, lipids, and nucleic acids. A comprehensive review of the literature from databases such as PubMed, Scopus, and Web of Science reveals insights into the formation, release, and uptake of EVs in CC, underscoring their potential as diagnostic and prognostic biomarkers. The review also explores therapeutic strategies targeting EVs, which include modifying their release and content, utilizing them for drug delivery, genetically altering their contents, and inhibiting key cachexia pathways. Understanding the role of EVs in CC opens new avenues for diagnostic and therapeutic approaches, potentially mitigating the syndrome’s impact on patient survival and quality of life.

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Section: Evs and Pathogenesis Of CCmentioning

confidence: 99%

Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons

Wang,

Ding

2024

J Transl Med

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“…Such defects include loss of skeletal muscle insulin sensitivity 24 and a perturbed balance between myocellular protein synthesis and protein breakdown that favors muscle protein loss 25 . Since insulin resistance and perturbed proteostasis are both associated with inflammation 26 and oxidative stress, 27 these cellular defects are also likely functionally related to the observed changes in mitochondrial activity. Primary sarcopenia is further characterized by hormonal changes, 28 a decline in the number of skeletal muscle satellite cells, 29–32 muscle fiber type transitions, 33 the loss of neuromuscular junctions, 34 and by fat infiltration within and between muscle fibers 2 .…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial involvement in sarcopenia

Affourtit,

Carré

2024

Acta Physiologica

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Sarcopenia lowers the quality‐of‐life for millions of people across the world, as accelerated loss of skeletal muscle mass and function contributes to both age‐ and disease‐related frailty. Physical activity remains the only proven therapy for sarcopenia to date, but alternatives are much sought after to manage this progressive muscle disorder in individuals who are unable to exercise. Mitochondria have been widely implicated in the etiology of sarcopenia and are increasingly suggested as attractive therapeutic targets to help restore the perturbed balance between protein synthesis and breakdown that underpins skeletal muscle atrophy. Reviewing current literature, we note that mitochondrial bioenergetic changes in sarcopenia are generally interpreted as intrinsic dysfunction that renders muscle cells incapable of making sufficient ATP to fuel protein synthesis. Based on the reported mitochondrial effects of therapeutic interventions, however, we argue that the observed bioenergetic changes may instead reflect an adaptation to pathologically decreased energy expenditure in sarcopenic muscle. Discrimination between these mechanistic possibilities will be crucial for improving the management of sarcopenia.

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“…Moreover, there is an increase in the expression of two skeletal muscle-specific E3 ubiquitin ligases: muscle-specific ring finger protein 1 (MuRF1) and muscle atrophy F-box protein (Atrogin-1). During this period, several atrophy pathways are triggered in skeletal muscle: (1) mitochondrial disorders can lead to decreased mitochondrial membrane potential and excessive production of ROS, which in turn activate oxidative stress, inflammation, protein synthesis, and degradation-related signaling pathways, triggering muscle atrophy programs [ 23 , 24 ]. (2) Various non-coding RNAs accelerate skeletal muscle atrophy by targeting mitochondrial dynamics and mitophagy-related proteins, resulting in reduced mitochondrial numbers and dysfunction [ 25 – 28 ] (Fig.…”

Section: Introductionmentioning

confidence: 99%

The role of mitochondrial dynamics and mitophagy in skeletal muscle atrophy: from molecular mechanisms to therapeutic insights

Lei,

Gan,

Qiu

et al. 2024

Cell Mol Biol Lett

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Skeletal muscle is the largest metabolic organ of the human body. Maintaining the best quality control and functional integrity of mitochondria is essential for the health of skeletal muscle. However, mitochondrial dysfunction characterized by mitochondrial dynamic imbalance and mitophagy disruption can lead to varying degrees of muscle atrophy, but the underlying mechanism of action is still unclear. Although mitochondrial dynamics and mitophagy are two different mitochondrial quality control mechanisms, a large amount of evidence has indicated that they are interrelated and mutually regulated. The former maintains the balance of the mitochondrial network, eliminates damaged or aged mitochondria, and enables cells to survive normally. The latter degrades damaged or aged mitochondria through the lysosomal pathway, ensuring cellular functional health and metabolic homeostasis. Skeletal muscle atrophy is considered an urgent global health issue. Understanding and gaining knowledge about muscle atrophy caused by mitochondrial dysfunction, particularly focusing on mitochondrial dynamics and mitochondrial autophagy, can greatly contribute to the prevention and treatment of muscle atrophy. In this review, we critically summarize the recent research progress on mitochondrial dynamics and mitophagy in skeletal muscle atrophy, and expound on the intrinsic molecular mechanism of skeletal muscle atrophy caused by mitochondrial dynamics and mitophagy. Importantly, we emphasize the potential of targeting mitochondrial dynamics and mitophagy as therapeutic strategies for the prevention and treatment of muscle atrophy, including pharmacological treatment and exercise therapy, and summarize effective methods for the treatment of skeletal muscle atrophy.

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Oxidative stress: Roles in skeletal muscle atrophy

Cited by 63 publications

References 176 publications

Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons

Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons

Mitochondrial involvement in sarcopenia

The role of mitochondrial dynamics and mitophagy in skeletal muscle atrophy: from molecular mechanisms to therapeutic insights

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