GILS1 alleviates cell senescence and renal fibrosis through PGC-1a-mediated mitochondrial quality control in kidney aging
Mitochondria take part in a network of intracellular processes that regulate homeostasis. Mitochondrial dysfunction is implied as a crucial factor in age-related chronic kidney disease. Gli-like transcription factor 1 (GLIS1) is enriched in physiology aging kidneys and decreased in aged human kidney that was confirmed in our previous research, however, the correlation between mitochondrial disturbances and GLIS1-driven kidney aging are not clearly clarified. Thus, we investigated the role of GLIS1 in the homeostasis of mitochondrial quality control both in vivo and in vitro. The lower expression of GLIS1 was identified in natural and accelerated aged models, accompanied by the mitochondrial quality control (MQC) dysfunctions, including enhanced mitochondrial fission, reduced mitochondrial biogenesis and mitophagy. After the induction of kidney aging, adeno-associated virus carrying GLIS1 over-expression or vector were delivered to the mice. Overall design: 8-week-old C57BL/6 mice were administered subcutaneous injections of D-gal (500mg/kg/day) for 8 weeks, which is a well-established aging model both in vitro and in vivo we then performed gene expression profiling analysis using data obtained from RNA-seq of 6 different tissue of kidney.