ArticleJournal of inflammation (London, England)2026
Ubiquitination-mediated PRDX2 alleviates intervertebral disc degeneration via restraining TBHP-induced nucleus pulposus cell apoptosis, ferroptosis and ECM degradation.
Article in Journal of inflammation (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPeroxiredogenase 2 (PRDX2) has been confirmed to be downregulated in patients with intervertebral disc degeneration (IDD). However, the role and mechanism of PRDX2 in the progression of IDD are still unclear.
methodsTert-butyl hydroperoxide (TBHP)-induced nucleus pulposus (NP) cells were used to construct IDD conditions. qRT-PCR or western blot was used to detect the expression levels of PRDX2, ubiquitin-specific protease 11 (USP11), ferroptosis-related markers and extracellular matrix (ECM)-related proteins. CCK8 assay, TUNEL assay and detection of ferroptosis-related markers were performed to examine cell viability, apoptosis and ferroptosis. Co-IP assay and ubiquitination assay were used to explore the regulation of USP11 on PRDX2.
resultsThe expression levels of PRDX2 and USP11 were reduced in IDD patients and TBHP-induced NP cells. PRDX2 overexpression repressed TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation. Moreover, our study found that USP11 stabilized the protein expression of PRDX2 by decreasing its ubiquitination. In addition, USP11 overexpression inhibited TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, while these effects were reversed by PRDX2 knockdown.
conclusionUSP11-mediated deubiquitination of PRDX2 might alleviate IDD progression by inhibiting TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, providing a potential intervention target worthy of further research for IDD.
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