ArticleCell & bioscience2017
Vincristine alleviates adriamycin-induced nephropathy through stabilizing actin cytoskeleton.
Article in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 34 citations in OpenAlex.
- Response to the Letter to the Editor Entitled "Revisiting Vincristine for FSGS: Proof-of-Mechanism Arrives, but Whom Should we Treat?"Kidney international reports · 2026Article
- Vincristine Treatment Protects Against Podocyte Damage in Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Adriamycin-induced nephropathy models: elucidating CKD pathophysiology and advancing therapeutic strategies.Experimental animals · 2025Review
- Pulsed Vincristine Therapy in Steroid-Resistant Nephrotic Syndrome.BioMed research international · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antimicrotubule agent vincristine (VCR) has long been known as an alternative treatment for frequent relapse nephrotic syndrome and steroid-dependent nephrotic syndrome (SDNS). However, the mechanism is unknown. Here we found that VCR at a dosage much lower than that as an antimicrotubule agent can alleviate adriamycin (ADR)-induced proteinuria and podocyte foot process effacement. In cultured podocytes, VCR prevents ADR-induced actin fiber disorganization. In both in vitro and in vivo models, VCR suppresses ADR-induced overexpression of α3β1 integrin and focal adhesion kinase (FAK). These data suggest that VCR may relieve ADR-induced nephropathy through inhibiting injury-induced activation of integrin outside-in signaling to prevent actin cytoskeleton remodeling. Hence, our work reveals a novel role of VCR in regulating actin fiber assembly and provides first evidence on the therapeutic mechanism of VCR on nephrotic syndrome.
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Registered trials
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