MT2A promotes angiogenesis in chronically ischemic brains through a copper-mitochondria regulatory mechanism.

ABSTRACT:

Background

Approximately half of patients with chronic ischemic cerebrovascular disease (CICD) exhibit poor revascularization. Metallothionein 2 A (MT2A) has a high affinity for metal ions and is potentially capable of chelating toxic copper ions to alleviate the impairment of angiogenesis. Therefore, we hypothesized that MT2A could promote angiogenesis in chronically ischemic brains by neutralizing excessive copper ions during copper overload (CPO).

Methods

We first collected dura matter (DM) samples from CICD patients and examined the expression of cuproptosis-related genes (DLAT, FDX1, and SDHB) to confirm the inhibitory effect of CPO on angiogenesis. Then, we treated human umbilical vein endothelial cells (HUVECs) with different concentrations of elesclomol and CuCl

SUBMITTER: Mo N 

PROVIDER: S-EPMC11800420 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature