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Moreover, according to the CMAP database, we identified isoliquiritigenin (ISL) as an agent to inhibit ITGB3. ITGB3 overexpression could induce p53 pathway activation and the secretion of TGF-β, which, in turn, resulted in senescent and profibrotic phenotype change in cultured tubular cells. Here, we report that integrin β3 (ITGB3) expression was increased in tubular cells and positively correlated with fibrosis degree in CKD patients. Tubular cell senescence is a common biologic process and contributes to the progression of chronic kidney disease (CKD) however, the molecular mechanisms regulating tubular cell senescence are poorly understood. 4Department of Clinical Genetics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.3Center for Kidney Disease, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.2Department of Nephrology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.1National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University Medical School, Nanjing, China.Shen Li 1,2†, Song Jiang 1†, Qingyan Zhang 2, Bo Jin 2, Daoyuan Lv 1, Wenju Li 1, Min Zhao 2, Chunming Jiang 2*, Chunsun Dai 3,4* and Zhihong Liu 1*