Endothelial CHOP as a central mechanism in renovascular hypertension-induced vascular endothelial dysfunction and cardiac fibrosis.

ABSTRACT:

Objective

In this study, we sought to determine the significant impact of the vascular endothelial endoplasmic reticulum (ER) stress C/EBP homologous protein (CHOP) in renovascular hypertension-induced vascular endothelial dysfunction and cardiac fibrosis.

Approach and results

Eight-week-old male and female CHOP^flox/flox and EC^CHOP-/- mice were randomly divided into eight groups with and without 2-Kidney-1-Clip (2K1C) surgery for four weeks. Body weight, systolic blood pressure, running performance, cardiac hypertrophy and fibrosis, lung edema, inflammation, vascular endothelial function, and signaling were assessed. For the mechanism, we utilized human coronary endothelial cells, both with and without CHOP down-regulation, and then stimulated them with

SUBMITTER: Srinivas B 

PROVIDER: S-EPMC12165939 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature