粒体自噬
生物
线粒体
变性(医学)
氧化应激
衰老
细胞生物学
病理生理学
程序性细胞死亡
细胞凋亡
平衡
细胞器
椎间盘
自噬
神经科学
生物信息学
病理
内分泌学
解剖
遗传学
医学
腰椎
作者
Cong Zhang,Xin Peng,Feng Wang,Zhi‐Yang Xie,Lu Chen,Xiaotao Wu
标识
DOI:10.1089/dna.2021.1012
摘要
Low back pain (LBP) is a common disorder in orthopedic outpatients, affecting people of all ages, and some patients may develop chronic LBP. As a complex organelle, mitochondria are not only energy workstations but also regulate cell senescence, apoptosis, and homeostasis. Mitochondrial dysfunction promotes disk degeneration by affecting a variety of pathophysiological processes, including oxidative stress, mitophagy, mitochondrial homeostasis, cellular senescence, and cell death. We review the molecular mechanisms underlying the relationship between mitochondrial dysfunction and intervertebral disk degeneration (IDD) to provide a theoretical basis for IDD treatment using pharmacological or tissue-engineering approaches.
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