Objectives: Dysfunctional mitochondria induce inflammation of the kidney, which is the major mediator of pro-aging process of chronic kidney disease. PTEN-induced kinase 1(PINK1) is a protein involved in the quality control of mitochondria and plays a role in regulating mitochondrial dysfunction. Although it is known that the mitochondrial DNA release promoted by PINK1 deficiency stimulates cyclic GMPAMP synthase (cGAS) - stimulator of interferon genes (STING) pathway eventually resulting in the inflammatory response, the role of PINK1 and cGAS-STING pathway in renal aging has not yet been clarified. This study aimed to investigate the relationship between PINK1 and renal aging especially through the cGAS-STING pathway. Methods: To determine the role of PINK1 on renal aging process, renal fibrosis and tubular injury were compared in 4- and 24-month-old wild type (Pink1+/+) and PINK1 knockout (Pink1-/-) mice. To establish in vitro senescence model, H2O2 treatment on human renal proximal cells (HKC-8) was used. The changes of gene expression levels related to PINK1 were analyzed by RNA sequencing, applying transcriptomic and metabolomic analyses. Results: The renal fibrosis and tubular injury were significantly aggravated in 24-month-old Pink1-/- mice compared to 24-month-old Pink1+/+ mice. Western blot and RT-qPCR confirmed remarkably increased senescence markers and SASPs in 24-month Pink1-/- mice and senescence-induced HKC-8 cells. The RNA sequencing of mice kidneys showed that inflammation-related pathways significantly increased in 24 month Pink1-/-mice, and transcriptomic and metabolomic analyses showed that PINK1 has association with mitochondrial metabolism dysregulation. Finally, the STING pathway was significantly activated in 24-month Pink1-/- mice and senescence-induced HKC-8 cells, which was inhibited by a specific inhibitor of STING, H-151. Conclusions: In conclusion, PINK1 is associated with renal aging, and the dysregulation of mitochondria caused by PINK1 deficiency might lead to aging-related inflammatory responses through the cGAS-STING pathway.