The current insights of mitochondrial hormesis in the occurrence and treatment of bone and cartilage degeneration.

IF 4.3 2区 生物学 Q1 BIOLOGY
Wacili Da, Quan Chen, Bin Shen
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引用次数: 0

Abstract

It is widely acknowledged that aging, mitochondrial dysfunction, and cellular phenotypic abnormalities are intricately associated with the degeneration of bone and cartilage. Consequently, gaining a comprehensive understanding of the regulatory patterns governing mitochondrial function and its underlying mechanisms holds promise for mitigating the progression of osteoarthritis, intervertebral disc degeneration, and osteoporosis. Mitochondrial hormesis, referred to as mitohormesis, represents a cellular adaptive stress response mechanism wherein mitochondria restore homeostasis and augment resistance capabilities against stimuli by generating reactive oxygen species (ROS), orchestrating unfolded protein reactions (UPRmt), inducing mitochondrial-derived peptides (MDP), instigating mitochondrial dynamic changes, and activating mitophagy, all prompted by low doses of stressors. The varying nature, intensity, and duration of stimulus sources elicit divergent degrees of mitochondrial stress responses, subsequently activating one or more signaling pathways to initiate mitohormesis. This review focuses specifically on the effector molecules and regulatory networks associated with mitohormesis, while also scrutinizing extant mechanisms of mitochondrial dysfunction contributing to bone and cartilage degeneration through oxidative stress damage. Additionally, it underscores the potential of mechanical stimulation, intermittent dietary restrictions, hypoxic preconditioning, and low-dose toxic compounds to trigger mitohormesis, thereby alleviating bone and cartilage degeneration.

线粒体激素作用在骨和软骨退行性病变的发生和治疗方面的最新研究成果。
人们普遍认为,衰老、线粒体功能障碍和细胞表型异常与骨和软骨的退化密切相关。因此,全面了解线粒体功能的调控模式及其内在机制,有望缓解骨关节炎、椎间盘退化和骨质疏松症的进展。线粒体荷尔蒙发生(又称线粒体激素发生)是一种细胞适应性应激反应机制,线粒体通过产生活性氧(ROS)、协调未折叠蛋白反应(UPRmt)、诱导线粒体衍生肽(MDP)、激发线粒体动态变化和激活线粒体吞噬来恢复平衡和增强抵抗刺激的能力,所有这些都是由低剂量的应激物引起的。不同性质、强度和持续时间的刺激源会引起不同程度的线粒体应激反应,随后激活一种或多种信号通路,启动有丝分裂。本综述特别关注与有丝分裂相关的效应分子和调控网络,同时还仔细研究了线粒体功能障碍通过氧化应激损伤导致骨和软骨退化的现有机制。此外,它还强调了机械刺激、间歇性饮食限制、缺氧预处理和低剂量有毒化合物引发有丝分裂的潜力,从而缓解骨和软骨退化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biological Research
Biological Research 生物-生物学
CiteScore
10.10
自引率
0.00%
发文量
33
审稿时长
>12 weeks
期刊介绍: Biological Research is an open access, peer-reviewed journal that encompasses diverse fields of experimental biology, such as biochemistry, bioinformatics, biotechnology, cell biology, cancer, chemical biology, developmental biology, evolutionary biology, genetics, genomics, immunology, marine biology, microbiology, molecular biology, neuroscience, plant biology, physiology, stem cell research, structural biology and systems biology.
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