Mitophagy-mediated inflammation and oxidative stress contribute to muscle wasting in cancer cachexia.

cancer cachexia inflammation mitophagy oxidative stress skeletal muscle wasting

Journal

Journal of clinical biochemistry and nutrition
ISSN: 0912-0009
Titre abrégé: J Clin Biochem Nutr
Pays: Japan
ID NLM: 8700907

Informations de publication

Date de publication:
Jul 2023
Historique:
received: 11 01 2023
accepted: 12 02 2023
medline: 3 8 2023
pubmed: 3 8 2023
entrez: 3 8 2023
Statut: ppublish

Résumé

Cancer cachexia is commonly seen in patients with malignant tumors, which usually leads to poor life quality and negatively affects long-term prognosis and survival. Mitochondria dysfunction and enhanced autophagy are well-established to play an important role in skeletal muscle wasting. However, whether mitophagy is engaged in the pathogenesis of cancer cachexia requires further investigation. This study comprised a clinical study and animal experimentation. Clinical data such as CT images and laboratory results were obtained and analyzed. Then mice model of cancer cachexia and mitophagy inhibition were established. Data including skeletal muscle mass and function, mitochondria structure and function, inflammatory factors as well as ROS concentration. Mitophagy was enhanced in cancer cachexia patients with increased inflammatory factors. Greater disruption of skeletal muscle fiber and mitochondria structure were seen in cancer cachexia, with a higher level of inflammatory factors and ROS expression in skeletal muscle. Meanwhile, ATP production was undermined, indicating a close relationship with mitophagy, inflammation, and oxidative stress in the skeletal muscle of cancer cachexia mice models. In conclusion, mitophagy is activated in cancer cachexia and may play a role in skeletal muscle atrophy, and inflammation and oxidative stress might participate in mitophagy-related skeletal muscle injury.

Identifiants

pubmed: 37534096
doi: 10.3164/jcbn.23-1
pii: DN/JST.JSTAGE/jcbn/23-1
pmc: PMC10390805
doi:

Types de publication

Journal Article

Langues

eng

Pagination

34-42

Informations de copyright

Copyright © 2023 JCBN.

Déclaration de conflit d'intérêts

No potential conflicts of interest were disclosed.  

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Auteurs

Zhige Zhang (Z)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Shanjun Tan (S)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Shuhao Li (S)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Yuxi Cheng (Y)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Junjie Wang (J)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Hao Liu (H)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Mingyue Yan (M)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Guohao Wu (G)

Department of General Surgery/Shanghai Clinical Nutrition Research Center, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai 200032, China.

Classifications MeSH