ArticleJournal of cellular and molecular medicine2024
MST1 knockdown inhibits osteoarthritis progression through Parkin-mediated mitophagy and Nrf2/NF-κB signalling pathway.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- MST1/Drp1 axis mediates microglia pro-inflammatory activation following cerebral ischemia-reperfusion injury.Scientific reports · 2026Article
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
- Administration with carnosic acid alleviates the development of osteoarthritis by attenuating macrophage polarization-mediated inflammation and cartilage oxidative damage and degradation via regulating Nrf2/NF-kB axis.Frontiers in immunology · 2026Article
- MST1 modulates inflammatory responses by targeting the NF-κB/NLRP3 pathway in LPS-induced acute lung injury.Histochemistry and cell biology · 2025Article
- MST1 enhances radio-sensitivity in glioblastoma by suppressing autophagy and promoting apoptosis.American journal of cancer research · 2025Article
- MST1 knockdown inhibits osteoarthritis progression through Parkin-mediated mitophagy and Nrf2/NF-κB signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Investigating the shared genetic architecture of osteoarthritis and frailty: a genome-wide cross-trait analysis.American journal of nuclear medicine and molecular imaging · 2024Article
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Authors and funding
9 authors.
Funding
Abstract
Osteoarthritis (OA) is a complicated disease that involves apoptosis and mitophagy. MST1 is a pro-apoptotic factor. Hence, decreasing its expression plays an anti-apoptotic effect. This study aims to investigate the protective effect of MST1 inhibition on OA and the underlying processes. Immunofluorescence (IF) was used to detect MST1 expression in cartilage tissue. Western Blot, ELISA and IF were used to analyse the expression of inflammation, extracellular matrix (ECM) degradation, apoptosis and mitophagy-associated proteins. MST1 expression in chondrocytes was inhibited using siRNA and shRNA in vitro and in vivo. Haematoxylin-Eosin, Safranin O-Fast Green and alcian blue staining were used to evaluate the therapeutic effect of inhibiting MST1. This study discovered that the expression of MST1 was higher in OA patients. Inhibition of MST1 reduced inflammation, ECM degradation and apoptosis and enhanced mitophagy in vitro. MST1 inhibition slows OA progression in vivo. Inhibiting MST1 suppressed apoptosis, inflammation and ECM degradation via promoting Parkin-mediated mitophagy and the Nrf2-NF-κB axis. The results suggest that MST1 is a possible therapeutic target for the treatment of osteoarthritis as its inhibition delays the progression of OA through the Nrf2-NF-κB axis and mitophagy.
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Registered trials
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