#3620 AGING-RELATED RENAL FIBROSIS WAS ALLEVIATED VIA CONSERVING MITOCHONDRIAL FUNCTION AND AUTOPHAGY IN NLRP3 KO MICE

Abstract Background and Aims Nod-like receptor family, pyrin domain containing-3 (NLRP3) activation in kidney diseases contributes to aggravating disease progression fibrosis. However, the role of NLRP3 renal aging is not clear. This study was designed identify whether KO mice could be protected from aging. Method counterpart wild-type (WT) were used at different ages (3 months, 12 24 months). Plasma, urine, kidneys collected. Results Plasma creatinine blood urea nitrogen (BUN) increased with aging, while BUN significantly decreased old (24M) compared WT mice. ablation contributed decreasing tubular vacuolization, tubulointerstitial fibrosis, atypical autophagosomes In line it, fibrosis markers, such as connective tissue growth factor, fibronectin alleviated RT-PCR tests. Immunoblot results showed that autophagy mitochondrial biogenesis addition, phosphorylated AMP-activated protein kinase persoxisome proliferator-activated gamma coactivator 1α Transcriptional expression data using RNA bulk sequencing augmentation Conclusion absence prevented aging-related via maintaining autophagy.