Fig. 4: Enhancing autophagy could reduce NLRP3 inflammasome activation and podocyte injury.

A The regulatory relationship between CD36 and MAP1LC3B was explored by CRISPR/Cas9 technology and subsequent western blot analysis. B Western blotting of autophagy markers LC3B and p62 in human podocytes with treatment of IgG-LN (500 μg/ml; 72 h), compared to no treatment (Untreated vs. IgG-LN). C Western blot analysis of LC3B, p62, Nephrin, Podocin, NLRP3, Caspase1, Cleaved-Caspase1, and IL-1β in human podocytes under different treatments (Untreated vs. IgG-LN; IgG-LN vs. MAP1LC3B KO + IgG-LN; MAP1LC3B KO + IgG-LN vs. MAP1LC3B KO + MAP1LC3B OE + IgG-LN). D Western blot analysis of LC3B, p62, Nephrin, Podocin, NLRP3, Caspase1, Cleaved-Caspase1, and IL-1β in human podocytes under different treatments (Untreated vs. IgG-LN; IgG-LN vs. rapamycin + IgG-LN; IgG-LN vs. 3-MA + IgG-LN). E Representatives of Annexin V - PI double-staining in different groups and quantitative of apoptosis was shown in histogram with mean ± SD from 3 experiments (Untreated vs. IgG-LN; IgG-LN vs. rapamycin + IgG-LN; IgG-LN vs. 3-MA + IgG-LN). Cle-Caspase1: Cleaved-Caspase1. Data are expressed as the mean ± SD. *p < 0.05. **p < 0.01. ***p < 0.001.