Mitofusin-2 prevents skeletal muscle wasting in cancer cachexia
| Autor: | Qiu‑Lin Zhuang, Hai‑Yu Wang, Yu‑Song Han, Qiu Lei Xi, Jun Han, Ying Chen, Yi Jiang, Hai-Sheng Zhang, Guo Hao Wu, Bo Zhang, Jing Fang, Qing‑Yang Meng |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Cancer Research medicine.medical_specialty Biology Cachexia 03 medical and health sciences Gastrocnemius muscle 0302 clinical medicine Atrophy Internal medicine medicine Myocyte Wasting digestive oral and skin physiology Skeletal muscle Cancer Articles medicine.disease musculoskeletal system 030104 developmental biology Endocrinology medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis medicine.symptom C2C12 hormones hormone substitutes and hormone antagonists |
| Zdroj: | Oncology letters. 12(5) |
| ISSN: | 1792-1074 |
| Popis: | Cancer cachexia remains a leading cause of morbidity and mortality worldwide, despite extensive research and clinical trials. The prominent clinical feature of cancer cachexia is the continuous loss of skeletal muscle that cannot be fully reversed by conventional nutritional support, and that leads to progressive functional impairment. The mechanism underlying muscle loss in patients with cachexia is poorly understood. The present study analyzed 21 cancer patients with or without cachexia, and demonstrated that mitofusin-2 (Mfn2) was downregulated in the rectus abdominis of patients with cachexia, which was associated with body weight loss. In vitro cell experiments indicated that loss of Mfn2 was associated with atrophy of the C2C12 mouse myoblast cell line. Furthermore, in vivo animal experiments demonstrated that cachexia decreased gastrocnemius muscle mass and Mfn2 expression, and overexpression of Mfn2 in gastrocnemius muscle was able to partially attenuate cachexia-induced gastrocnemius muscle loss. The results of the present study suggested that Mfn2 is involved in cachexia-induced muscle loss and may serve as a potential target for therapy of cachexia. |
| Databáze: | OpenAIRE |
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