This study investigates the role of zinc transporter 8 (ZnT8) in protecting renal tubular epithelial cells from apoptosis in diabetic kidney disease (DKD). Using ZnT8 Knockout (ZnT8-KO) mice and STZ-induced diabetic models, the researchers demonstrated that ZnT8 deficiency exacerbates renal injury, increases apoptosis, and elevates proinflammatory cytokine levels. In vitro, overexpression of ZnT8 in NRK-52E cells reduced high glucose-induced apoptosis and inflammation via upregulation of TNFAIP3 and suppression of the NF-κB pathway.
ZnT8 plays a protective role in DKD by inhibiting apoptosis and inflammation in renal tubular epithelial cells through the TNFAIP3-NF-κB signaling pathway. Its deficiency leads to aggravated renal injury, highlighting its potential as a therapeutic target.
ZnT8 Knockout (ZnT8-KO) mice and STZ-induced diabetic mouse models, utilized to assess the impact of ZnT8 deficiency on renal tubular epithelial cell apoptosis and inflammation in DKD.
Diabetic kidney disease, Renal tubular epithelial cells, Apoptosis, Inflammation, Zinc transporter 8
Knockout mouse model, STZ-induced diabetes, Gene overexpression, NF-κB pathway analysis
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