椎间盘
自噬
MAPK/ERK通路
变性(医学)
细胞生物学
信号转导
氧化应激
炎症
p38丝裂原活化蛋白激酶
衰老
细胞外基质
阿达姆斯
医学
生物信息学
生物
病理
细胞凋亡
基质金属蛋白酶
免疫学
解剖
内科学
遗传学
金属蛋白酶
血栓反应素
作者
Xingmin Zhang,Zilin Zhang,Xiaosong Zou,Yongjie Wang,Jinwei Qi,Song Han,Jingguo Xin,Zhi Zheng,Wei Lin,Tianhui Zhang,S. Zhang
标识
DOI:10.3389/fcell.2023.1324561
摘要
Intervertebral disc (IVD) degeneration (IDD) is a worldwide spinal degenerative disease. Low back pain (LBP) is frequently caused by a variety of conditions brought on by IDD, including IVD herniation and spinal stenosis, etc. These conditions bring substantial physical and psychological pressure and economic burden to patients. IDD is closely tied with the structural or functional changes of the IVD tissue and can be caused by various complex factors like senescence, genetics, and trauma. The IVD dysfunction and structural changes can result from extracellular matrix (ECM) degradation, differentiation, inflammation, oxidative stress, mechanical stress, and senescence of IVD cells. At present, the treatment of IDD is basically to alleviate the symptoms, but not from the pathophysiological changes of IVD. Interestingly, the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway is involved in many processes of IDD, including inflammation, ECM degradation, apoptosis, senescence, proliferation, oxidative stress, and autophagy. These activities in degenerated IVD tissue are closely relevant to the development trend of IDD. Hence, the p38 MAPK signaling pathway may be a fitting curative target for IDD. In order to better understand the pathophysiological alterations of the intervertebral disc tissue during IDD and offer potential paths for targeted treatments for intervertebral disc degeneration, this article reviews the purpose of the p38 MAPK signaling pathway in IDD.
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