AMPK alleviates high uric acid-induced Na+-K+-ATPase signaling impairment and cell injury in renal tubules

Kidney damage: Identifying mechanisms behind uric acid effects High serum levels of uric acid cause kidney tissue damage through cellular processes that have now been identified by researchers in China. Uric acid is a common component of urine, but causes damage if it is present in high levels in the blood (hyperuricemia). While investigating the mechanisms behind hyperuricemia, Zhibin Ye and co-workers at Fudan University in Shanghai recently showed that impairment of the Na+-K+-ATPase (NKA) signaling pathway, which regulates uric acid transportation through the kidneys, is a crucial feature of renal damage progression. The team have now shown that NKA is regulated by the AMP-activated protein kinase (AMPK) pathway, and that AMPK is enriched during the initial phases of hyperuricemia. Studies on rat models indicated that sustained AMPK activation restored NKA signaling, limiting damage from hyperuricemia.