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骨骼肌丢失的分子机制及其天然资源预防措施

Molecular mechanism of skeletal muscle loss and its prevention by natural resources.

作者信息

Kim Jin Tae, Jeon Dong Hyeon, Lee Hong Jin

机构信息

Department of Food Science and Biotechnology, Chung-Ang University, Anseong, 17546 South Korea.

GreenTech-Based Food Safety Research Group, BK21 Four, Chung-Ang University, Anseong, 17546 South Korea.

出版信息

Food Sci Biotechnol. 2024 Aug 16;33(15):3387-3400. doi: 10.1007/s10068-024-01678-x. eCollection 2024 Dec.

Abstract

A skeletal muscle disorder has drawn attention due to the global aging issues. The loss of skeletal muscle mass has been suggested to be from the reduced muscle regeneration by dysfunction of muscle satellite cell/fibro-adipogenic progenitor cells and the muscle atrophy by dysfunction of mitochondria, ubiquitin-proteasome system, and autophagy. In this review, we highlighted the underlying mechanisms of skeletal muscle mass loss including Notch signaling, Wnt/β-catenin signaling, Hedgehog signaling, AMP-activated protein kinase (AMPK) signaling, and mammalian target of rapamycin (mTOR) signaling. In addition, we summarized accumulated studies of natural resources investigating their roles in ameliorating the loss of skeletal muscle mass and demonstrating the underlying mechanisms in vitro and in vivo. In conclusion, following the studies of natural resources exerting the preventive activity in muscle mass loss, the signaling-based approaches may accelerate the development of functional foods for sarcopenia prevention.

摘要

由于全球老龄化问题,骨骼肌疾病已引起关注。骨骼肌质量的丧失被认为是由于肌肉卫星细胞/纤维脂肪生成祖细胞功能障碍导致肌肉再生减少,以及线粒体、泛素-蛋白酶体系统和自噬功能障碍导致肌肉萎缩。在本综述中,我们重点介绍了骨骼肌质量丧失的潜在机制,包括Notch信号通路、Wnt/β-连环蛋白信号通路、Hedgehog信号通路、AMP激活蛋白激酶(AMPK)信号通路和雷帕霉素靶蛋白(mTOR)信号通路。此外,我们总结了对天然资源的累积研究,这些研究调查了它们在改善骨骼肌质量丧失方面的作用,并在体外和体内证明了其潜在机制。总之,在对天然资源在预防肌肉质量丧失方面的预防活性进行研究之后,基于信号通路的方法可能会加速用于预防肌肉减少症的功能性食品的开发。

相似文献

1
Molecular mechanism of skeletal muscle loss and its prevention by natural resources.骨骼肌丢失的分子机制及其天然资源预防措施
Food Sci Biotechnol. 2024 Aug 16;33(15):3387-3400. doi: 10.1007/s10068-024-01678-x. eCollection 2024 Dec.

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