ArticleScientific reports2019
Gcm1 is involved in cell proliferation and fibrosis during kidney regeneration after ischemia-reperfusion injury.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 13 citations in OpenAlex.
- The key role of miR‑378 in kidney diseases (Review).Molecular medicine reports · 2025Review
- Identification of conserved skeletal enhancers associated with craniosynostosis risk genes.Human molecular genetics · 2024Article
- IL-17C neutralization protects the kidney against acute injury and chronic injury.EBioMedicine · 2023Article
- Blocking cell cycle progression through CDK4/6 protects against chronic kidney disease.JCI insight · 2022Article
- Systematic Investigations on the Metabolic and Transcriptomic Regulation of Lactate in the Human Colon Epithelial Cells.International journal of molecular sciences · 2022Article
- The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury.Cell death discovery · 2022Review
- Twist1 regulates macrophage plasticity to promote renal fibrosis through galectin-3.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- The protective function of miR-378 in the ischemia-reperfusion injury during renal transplantation and subsequent interstitial fibrosis of the renal allograft.International urology and nephrology · 2020Article
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7 authors at 1 institution in 1 country.
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Abstract
In acute kidney injury (AKI), the S3 segment of the proximal tubule is particularly damaged, as it is most vulnerable to ischemia. However, this region is also involved in renal tubular regeneration. To deeply understand the mechanism of the repair process after ischemic injury in AKI, we focused on glial cells missing 1 (Gcm1), which is one of the genes expressed in the S3 segment. Gcm1 is essential for the development of the placenta, and Gcm1 knockout (KO) is embryonically lethal. Thus, the function of Gcm1 in the kidney has not been analyzed yet. We analyzed the function of Gcm1 in the kidney by specifically knocking out Gcm1 in the kidney. We created an ischemia-reperfusion injury (IRI) model to observe the repair process after AKI. We found that Gcm1 expression was transiently increased during the recovery phase of IRI. In Gcm1 conditional KO mice, during the recovery phase of IRI, tubular cell proliferation reduced and transforming growth factor-β1 expression was downregulated resulting in a reduction in fibrosis. In vitro, Gcm1 overexpression promoted cell proliferation and upregulated TGF-β1 expression. These findings indicate that Gcm1 is involved in the mechanisms of fibrosis and cell proliferation after ischemic injury of the kidney.
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