The molecular mechanism underlying angiogenesis in a mouse model of chronic kidney disease after ischemic stroke.

Abstract

Objectives: The study aims to establish a reliable chronic kidney disease (CKD) mouse model by examining the effects of an adenine-containing diet on renal function and pathology. It also explores the impact of CKD on motor function and infarct volume following cerebral infarction and investigates the role of calcium in modulating the AMPK/SIRT1/HIF1-α signaling pathways.

Method: The CKD mouse model was induced through an adenine-enriched diet. Renal function impairment was assessed by analyzing blood samples for creatinine and blood urea nitrogen levels at 0 and 6 weeks. Pathologic changes in renal tissue were examined. The study also evaluated motor function, infarct volume, survival rates, body weight changes, and functional assessments. Additionally, cerebral cortex angiogenesis was assessed in the context of ischemic stroke.

Result: The CKD mouse model showed significant renal tissue alterations, including luminal dilation, glomerular hypertrophy, fibrosis, and inflammatory infiltration. There was a notable reduction in angiogenic markers in the CKD group compared to controls. The study also found increased cerebral calcium levels and altered expression of AMPK, SIRT1, HIF1-α, and VEGF in the CKD group.

Conclusions: The research successfully created the CKD mouse model and emphasized the disease's many effects, including its influence on neurological disorders. The results provide an understanding of the molecular processes behind changes brought on by CKD and may have consequences for angiogenesis and signaling pathway-focused therapeutic approaches.