Mitigating sepsis-induced vascular endothelial dysfunction through Niban phosphorylation.

ABSTRACT:

Introduction

Endothelial dysfunction is a hallmark of sepsis pathophysiology, driven by inflammation, oxidative stress, and endoplasmic reticulum (ER) stress, leading to vascular abnormalities and organ failure. Niban, a multifunctional cellular stress response protein, regulates endothelial homeostasis, with its phosphorylation playing a critical role in mitigating ER stress. We hypothesized that sepsis-induced endothelial dysfunction in the aorta is driven by reduced Niban phosphorylation, which increases ER stress, but can be restored by NiPp, a cell-permeant phosphopeptide mimetic designed to replicate phosphorylated Niban.

Methods

Rats were subjected to a cecal slurry model of polymicrobial sepsis. Molecular markers of ER stress and Niban phosphorylation were analyzed u

SUBMITTER: Baer B 

PROVIDER: S-EPMC12912783 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature