Flavin containing monooxygenase 2 regulates renal tubular cell fibrosis and paracrine secretion via SMURF2 in AKI‑CKD transformation.

ABSTRACT: In the follow‑up of hospitalized patients with acute kidney injury (AKI), it has been observed that 15‑30% of these patients progress to develop chronic kidney disease (CKD). Impaired adaptive repair of the kidneys following AKI is a fundamental pathophysiological mechanism underlying renal fibrosis and the progression to CKD. Deficient repair of proximal tubular epithelial cells is a key factor in the progression from AKI to CKD. However, the molecular mechanisms involved in the regulation of fibrotic factor paracrine secretion by injured tubular cells remain incompletely understood. Transcriptome analysis and an ischemia‑reperfusion injury (IRI) model were used to identify the contribution of flavin‑containing monooxygenase 2 (FMO2) in AKI‑CKD. Lentivirus‑mediated overexpression of FMO2

SUBMITTER: Wang L 

PROVIDER: S-EPMC10558214 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature