Fig. 2

Senescent TECs accumulation after AKI drives the progression of CKD. Acute kidney injury induces cellular damage and DNA degradation in TECs. Maladaptive repair after AKI leads to TECs senescence. Senescent TECs accumulates in kidney with SASP, which mainly includes proinflammatory cytokines, growth factors, chemokines, and matrix remodeling enzymes. These proinflammatory and profibrotic molecules aggravate immune cells infiltration and tubular cell injury, leading to persistent tubulointerstitial inflammation, proliferation of fibroblasts, and excessive deposition of extracellular matrix, which leads to the exacerbation of renal injury and drives AKI to CKD. Senescent immune cells such as CD28⁻ T cells, CD14⁺CD16⁺ monocytes also aggravate chronic inflammation and ROS production in kidney, which promotes the progression of CKD