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

ABSTRACT: One of the mechanisms in hyperuricemia (HUA)-induced renal tubular injury is the impairment of Na⁺-K⁺-ATPase (NKA) signaling, which further triggers inflammation, autophagy, and mitochondrial dysfunction and leads to cell injury. Here, we used RNA sequencing to screen the most likely regulators of NKA signaling and found that the liver kinase B1(LKB1)/adenosine monophosphate (AMP)-activated protein kinase (AMPK)/ mammalian target of rapamycin (mTOR) pathway was the most abundantly enriched pathway in HUA. AMPK is a key regulator of cell energy metabolism; hence, we examined the effect of AMPK on HUA-induced dysregulation of NKA signaling and cell injury. We first detected AMPK activation in high uric acid (UA)-stimulated proximal tubular epithelial cells (PTECs). We f

SUBMITTER: Xiao J 

PROVIDER: S-EPMC6531502 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature