Bio: Gao Ming, a professor and doctoral supervisor at the Center for Eco-Environmental Research, Chinese Academy of Sciences. His research interests mainly focus on the health risks and related molecular toxicological mechanisms of heavy metals and new environmental pollutants. He has hosted several research funding from NSFC such as the National Excellent Young Scientist Fund Program and General Program of NSFC. He has published more than 30 SCI papers as the first or corresponding author, including Nature Communications, Nucleic Acids Research, Cell Discovery, Advanced Science, Nano Today, etc.

Abstract: Cadmium is a severe environmental pollutant that mainly targets kidney and causes kidney disease. However, the mechanism of cadmium-induced kidney disease is still unclear. Herein, we found that the cadmium content in the serum of patients with kidney disease was closely related to the degree of fibrosis. Further studies have shown that although long-term cadmium exposure does not lead to the occurrence of kidney fibrosis in mice, it can promote the progression of kidney fibrosis in Unilateral Ureteral Obstruction (UUO) model. Further genome sequencing and in vitro cell models found that Hippo pathway was activated in the renal of cadmium-exposed mice, suggesting that Hippo pathway promotes cadmium-induced kidney fibrosis. Further mechanism analysis revealed that cadmium exerts its profibrotic effect by affecting the activity of RAP2, an upstream regulatory molecule of Hippo pathway. In addition, the cadmium levels in the serum of patients with kidney disease were positively correlated with the content of downstream targets of the Hippo pathway. Taken together, our data suggest that targeting the Hippo pathway may effectively alleviate the progression of kidney fibrosis.