ArticleInternational urology and nephrology2018
Silencing of CXCL12 performs a protective effect on C5b-9-induced injury in podocytes.
Article in International urology and nephrology, 2018. 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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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
- Advances of berberine against metabolic syndrome-associated kidney disease: Regarding effect and mechanism.Frontiers in pharmacology · 2023Review
- Mechanism of action ofRenal failure · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePodocytes, terminal differentiation cell in glomerulu, are crucial to kidney-related diseases such as membranous nephropathy (MN). MN is characterized by podocyte injury and glomerular basement membrane thickening. This paper focused to investigate the expression of chemokine (C-X-C motif) ligand 12 (CXCL12) in MN patients and its possible role in podocyte injury.
methodsThrough the enzyme-linked immunosorbent assay, CXCL12 level in the serum and urine of MN patients was examined. Further, several assays of cell viability, apoptosis, quantitative real-time PCR and western blot were applied to explore the effects of CXCL12 in the model of podocyte injury.
resultsWe found a significant increase of CXCL12 in serum and urine of MN patients, which indicated that CXCL12 may be involved in the progression of MN. And in vitro C5b-9-induced podocyte injury model, the proliferation of podocytes was inhibited whereas CXCL12/CXCR4 and phosphorylated STAT3 (p-STAT3) were increased. Silencing of CXCL12 remarkably promoted cell proliferation, inhibited cell apoptosis and suppressed CXCL12/CXCR4, p-STAT3 and caspase 3. Consistently, STAT3 inhibitor and berberine (a CXCL12 antagonist) also reduced CXCL12 treatment-induced apoptosis.
conclusionsAll data suggested that silencing of CXCL12 had a protective effect on podocyte injury, which may be through inhibiting CXCL12/STAT3 signaling pathway.
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