ArticleInternational journal of biological sciences2024
Mechanistic study of celastrol-mediated inhibition of proinflammatory activation of macrophages in IgA nephropathy via down-regulating ECM1.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Diagnostic potential of B-cell translocation gene 2 in IgA nephropathy: Insights from molecular mechanisms.Journal of cell communication and signaling · 2026Article
- IGF2BP3 Overexpression Accelerates Osteoarthritis Progression by Promoting Glycolysis via mThe Kaohsiung journal of medical sciences · 2026Article
- Orally Administered Self-Microemulsifying Celastrol Alleviates Rheumatoid Arthritis by Modulating the Expression of TNF-α.Pharmaceutics · 2026Article
- M2 macrophages alleviate podocyte apoptosis induced by supernatant of glomerular mesangial cells with aIgA1 via targeting UCHL1.In vitro cellular & developmental biology. Animal · 2026Article
- Extracellular matrix protein 1 in cancer: multifaceted roles in tumor progression, prognosis, and therapeutic targeting.Archives of pharmacal research · 2025Review
- Renoprotective mechanisms of celastrol in high glucose-mediated HK-2 cell injury through inhibition of the PI3K/Akt/NF-κB signalling pathway.Biochemistry and biophysics reports · 2025Article
- Article
- The multifaceted role of post-translational modifications in macrophage polarization: from mechanisms to therapeutic targets.Frontiers in immunology · 2025Review
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Authors and funding
13 authors.
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Abstract
Increasing evidence suggests that the mononuclear/macrophage system is vital in amplifying the inflammatory cascade in IgA Nephropathy (IgAN). However, the pathogenic mechanism of macrophages in IgAN and targeted treatment strategies still need to be explored. This study found that botanical triterpene celastrol (CLT) effectively alleviated renal lesions, M1-like macrophage infiltration, inflammatory factors production, and improved renal function in IgAN mice. We found that the renal macrophages of IgAN patients had high expression of ECM1, a crucial molecule involved in macrophage inflammatory polarization, positively correlated with the IgAN clinical severity. In murine macrophage Raw 264.7 cells, CLT inhibited macrophage M1-like polarization and the output of TNF-α and IL-6 by downregulating the ECM1/STAT5 pathway. Mechanistically, molecular docking, CESTA, and immunoprecipitation verified that CLT directly bound to ECM1 and increased the ubiquitination of ECM1. Collectively, these results illustrated that CLT inhibited proinflammatory macrophage in IgAN by directly targeting ECM1 to promote ubiquitination degradation of ECM1. Therefore, this study may provide a theoretical basis for exploring the pathogenesis of IgAN and identifying new perspectives for targeted therapy of IgAN.
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