Chitrangda Srivastava

Abstract Deficiency in GLI-similar 3 (GLIS3) in humans and mice causes polycystic kidney disease (PKD). We previously reported that Glis3-knockout (KO) kidneys undergo metabolic reprogramming and remain more reliant on aerobic glycolysis. Here, to understand the mechanism by which GLIS3 controls this process, we analyzed its role in regulating glycolytic gene expression using transcriptomics and cistromics.

1Emergency Intensive Care Unit, Ningxiang People’s Hospital Affiliated to Hunan University of Chinese Medicine, Changsha, China 2Emergency Department, Ningxiang People’s Hospital Affiliated to Hunan University of Chinese Medicine, Changsha, China Background: Lactate, as an essential clinical evaluation index of septic shock, is crucial in the incidence and progression of septic shock.