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Involvement of DJ-1 in the pathogenesis of intervertebral disc degeneration via hexokinase 2-mediated mitophagy
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논문 기본 정보

Type
Academic journal
Author
Lin Jialiang (Peking University Third Hospital) Wang Longjie (Peking University Third Hospital) Wu Yuhao (Wenzhou Medical University) Xiang Qian (Peking University Third Hospital) Zhao Yongzhao (Peking University Third Hospital) Zheng Xuanqi (Peking University Third Hospital) Jiang Shuai (Peking University Third Hospital)
Journal
KOREAN SOCIETY OF MEDICAL BIOCHEMISTRY AND MOLECULAR BIOLOGY Experimental and Molecular Medicine Experimental and Molecular Medicine Vol.56 KCI Accredited Journals SCI
Published
2024.3
Pages
1 - 13 (13page)
DOI
10.1038/s12276-024-01196-0

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Involvement of DJ-1 in the pathogenesis of intervertebral disc degeneration via hexokinase 2-mediated mitophagy
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Intervertebral disc degeneration (IDD) is an important pathological basis for degenerative spinal diseases and is involved in mitophagy dysfunction. However, the molecular mechanisms underlying mitophagy regulation in IDD remain unclear. This study aimed to clarify the role of DJ-1 in regulating mitophagy during IDD pathogenesis. Here, we showed that the mitochondrial localization of DJ-1 in nucleus pulposus cells (NPCs) first increased and then decreased in response to oxidative stress. Subsequently, loss- and gain-of-function experiments revealed that overexpression of DJ-1 in NPCs inhibited oxidative stress-induced mitochondrial dysfunction and mitochondria-dependent apoptosis, whereas knockdown of DJ-1 had the opposite effect. Mechanistically, mitochondrial translocation of DJ-1 promoted the recruitment of hexokinase 2 (HK2) to damaged mitochondria by activating Akt and subsequently Parkin-dependent mitophagy to inhibit oxidative stress-induced apoptosis in NPCs. However, silencing Parkin, reducing mitochondrial recruitment of HK2, or inhibiting Akt activation suppressed DJ-1-mediated mitophagy. Furthermore, overexpression of DJ-1 ameliorated IDD in rats through HK2-mediated mitophagy. Taken together, these findings indicate that DJ-1 promotes HK2-mediated mitophagy under oxidative stress conditions to inhibit mitochondria-dependent apoptosis in NPCs and could be a therapeutic target for IDD.

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