#6496 CYCLIN D1 AMELIORATES ACUTE KIDNEY INJURY BY IMPROVING FATTY ACID OXIDATION VIA AMPK PATHWAY

Abstract Background and Aims Acute Kidney Injury (AKI) is a critical condition that caused by the absence of oxygen during acute ischemic phase, leading to energy metabolism disturbance kidney tubular epithelial cell damage. Fatty Acid Oxidation (FAO) main source production renal proximal cells. Timely promoting FAO, increasing supplies energy, proliferation are essential improve injury. However, there no clinically recognized effective treatment for this. Cyclin D1(CCND1), member cycle family, plays vital role in proliferation. Our previous study showed CCND1 improved AKI FAO. This aimed investigate molecular basis involvement fatty acid oxidation AKI. Method was evaluated human cells (HK-2 cells) male C57BL/6J mice (wild type). We investigated protective using mouse model ischemia-reperfusion injury, which treated transferring CCND1-expressing plasmids type) ultrasound microbubble-mediated delivery. Eight-week-old were subjected bilateral artery occlusion 30min followed 24h reperfusion. proliferation, autophagy vitro vivo. In addition, we concentrations blood urea nitrogen creatinine, ultrastructure so on. Results vivo studies activation prevented AKI-induced lipid accumulation, tubule injury function declined after Compared test control, significantly (p<0.05) reduced creatinine. Kidney-specific overexpression increased promoted apoptosis. Mechanistically, activated AMPK pathway, expression phosphorylation AMP protein kinase (p-AMPK) upregulated On other hand, inhibiting worsened impairment FAO disturbed metabolism. Conclusion accumulation through active pathway (PTECs). Hence, restoring may offer novel therapeutic strategy treating