Hyperuricemia suppresses lumican, exacerbating adverse remodeling after myocardial infarction by promoting fibroblast phenotype transition.

ABSTRACT:

Background

Hyperuricemia is independently associated with a poor prognosis in patients with myocardial infarction (MI). Furthermore, MI induces activation of the repair response in local fibroblasts, resulting in extracellular matrix accumulation that generates a stable fibrotic scar in the infarcted area. However, researchers have not determined whether hyperuricemia affects fibroblast activation and its involvement in postinfarction cardiac remodeling.

Objectives

We aimed to trigger hyperuricemia by administering potassium oxonate in a mouse model of MI to evaluate the role of hyperuricemia in MI pathogenesis.

Methods

Microarray datasets and single-cell sequencing data from gout patients, heart failure patients, and model mice were used to identify the underlying me

SUBMITTER: Zhuang Z 

PROVIDER: S-EPMC11526644 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature