Nanoparticle-mediated overexpression of RacGAP1 protects against renal ischemia/reperfusion injury by maintaining mitochondrial homeostasis.

ABSTRACT: Acute kidney injury (AKI) is recognized as a critical clinical problem, and pharmacological therapeutic options for AKI remain limited. Our previous study confirmed that Rac GTPase-activating protein 1 (RacGAP1) effectively promoted the repair of tubular epithelial cells in vitro. Further investigation is needed to determine whether boosting the expression of RacGAP1 in vivo helps protect against AKI. Herein, lipid-coated calcium phosphate (LCP) nanoparticles loaded with RacGAP1 plasmids (pRacGAP1-LCP) were generated and subsequently characterized based on their size, zeta potential, and morphological features. Animal models of AKI induced by ischemia/reperfusion (I/R) injury (IRI) were established in C57BL/6 mice, and pRacGAP1-LCP was injected into the tail vein to explore the role of Rac

SUBMITTER: Zhou W 

PROVIDER: S-EPMC12751063 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature