The mTOR inhibition by Rapamycin limits LPS-induced acute kidney injury and ameliorates hallmarks of cellular senescence

ABSTRACT: Sepsis is a severe and dysregulated inflammatory disease that often precedes the development of acute kidney injury (AKI) with consequent worsening outcome. The main characteristics of sepsis-induced AKI include endothelial cell (EC) dysfunction, infiltration of inflammatory cells, glomerular thrombosis, and renal tubular epithelial cells (RTEC) injury. Numerous studies have demonstrated that mammalian target of rapamycin (mTOR) activation has been implicated in the initiation and progression of renal injury in course of sepsis. However, little is known, about the molecular basis of mTOR role in EC and RTEC dysfunction. Here, we evaluate whether mTOR inhibition by Rapamycin (Rp) as potential strategy to ameliorate renal function and dissected the molecular mechanisms involved. In a mouse

ORGANISM(S): Homo sapiens

SUBMITTER: Fabio Sallustio 

PROVIDER: E-MTAB-13396 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress