Unraveling the mechanisms of intervertebral disc degeneration: an exploration of the p38 MAPK signaling pathway
2024
Xingmin Zhang | Xingmin Zhang | Zilin Zhang | Zilin Zhang | Xiaosong Zou | Xiaosong Zou | Yongjie Wang | Yongjie Wang | Jinwei Qi | Jinwei Qi | Song Han | Song Han | Jingguo Xin | Jingguo Xin | Zhi Zheng | Zhi Zheng | Lin Wei | Lin Wei | Tianhui Zhang | Shaokun Zhang | Shaokun Zhang
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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