ArticleAmerican journal of physiology. Renal physiology2015
Increased expression of p21WAF1/CIP1 in kidney proximal tubules mediates fibrosis.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- CYFIP2 deficiency ameliorates renal interstitial fibrosis through attenuating tubular senescence in hypertensive nephropathy.Acta pharmacologica Sinica · 2026Article
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- DYRK2 drives renal fibrosis through CDK1-dependent G2/M phase dysregulation in tubular epithelial cells.Cellular & molecular biology letters · 2026Article
- Understanding and targeting senescence in kidney disease.Clinical kidney journal · 2025Review
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Lysosomal-Associated Protein Transmembrane 5, Tubular Senescence, and Progression of CKD.Journal of the American Society of Nephrology : JASN · 2024Article
- HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice.Nature communications · 2023Article
- Article
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- Reversal of the renal hyperglycemic memory in diabetic kidney disease by targeting sustained tubular p21 expression.Nature communications · 2022Article
- Loss of LAT1 sex-dependently delays recovery after caerulein-induced acute pancreatitis.World journal of gastroenterology · 2022Article
- A ferroptosis-related gene signature for graft loss prediction following renal allograft.Bioengineered · 2021Article
- Tubular Cell Cycle Response upon AKI: Revising Old and New Paradigms to Identify Novel Targets for CKD Prevention.International journal of molecular sciences · 2021Review
- Deciphering the Role of Heme Oxygenase-1 (HO-1) Expressing Macrophages in Renal Ischemia-Reperfusion Injury.Biomedicines · 2021Review
- Inhibitor of growth 2 regulates the high glucose-induced cell cycle arrest and epithelial-to-mesenchymal transition in renal proximal tubular cells.Journal of physiology and biochemistry · 2020Article
- Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage.Frontiers in immunology · 2020Review
- Cellular Senescence and Senotherapies in the Kidney: Current Evidence and Future Directions.Frontiers in pharmacology · 2020Review
- The Impact of p53 on Aristolochic Acid I-Induced Gene Expression In Vivo.International journal of molecular sciences · 2019Article
- Disruption of CUL3-mediated ubiquitination causes proximal tubule injury and kidney fibrosis.Scientific reports · 2019Article
- Acute Kidney Injury as a Condition of Renal Senescence.Cell transplantation · 2018Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue fibrosis is a major cause of death in developed countries. It commonly occurs after either acute or chronic injury and affects diverse organs, including the heart, liver, lung, and kidney. Using the renal ablation model of chronic kidney disease, we previously found that the development of progressive renal fibrosis was dependent on p21(WAF1/Cip1) expression; the genetic knockout of the p21 gene greatly alleviated this disease. In the present study, we expanded on this observation and report that fibrosis induced by two different acute injuries to the kidney is also dependent on p21. In addition, when p21 expression was restricted only to the proximal tubule, fibrosis after injury was induced in the whole organ. One molecular fibrogenic switch we describe is transforming growth factor-β induction, which occurred in vivo and in cultured kidney cells exposed to adenovirus expressing p21. Our data suggests that fibrosis is p21 dependent and that preventing p21 induction after stress could be a novel therapeutic target.
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