Cyclin B1 deficiency in renal tubular epithelial cells promotes kidney ageing and fibrosis in mice

After severe renal injury, renal tubular epithelial cells (TECs) will be arrested in G2/M phase, and the arrested cells will be aging, showing senescence related secretory phenotype (SASP), which mediates renal fibrosis by secreting fibrogenic cytokines. Cyclin B1 is an important protein that promotes G2/M phase transition of cell cycle. Its role in renal fibrosis mediated by G2/M arrest of TECs is unknown. The aim of this study was to investigate the role of cyclin B1 in renal fibrosis induced by TECs G2/M arrest and its mechanism Overall design: We compared the deletion of cyclin B1 in mouse renal tubular epithelial cells with that in the control group by sequencing genes to explore the role of cyclin B1 in renal fibrosis caused by G2/M cycle arrest of epithelial cells.