A sex-dependent role of Kv1.3 channels from macrophages in metabolic syndrome.

ABSTRACT:

Introduction

Coronary artery disease (CAD) is the foremost single cause of mortality and disability globally. Patients with type 2 diabetes (T2DM) have a higher incidence of CAD, and poorer prognosis. The low-grade inflammation associated to T2DM contributes to increased morbidity and worst outcomes after revascularization. Inflammatory signaling in the vasculature supports endothelial dysfunction, leukocyte infiltration, and macrophage activation to a metabolic disease (MMe) specific phenotype, which could contribute to the metabolic disorders and ascular damage in T2DM. We have previously found that K_v1.3 blockers inhibit the development of intimal hyperplasia, thereby preventing restenosis. This inhibition was enhanced in a mouse model of T2DM, where systemic K_v<

SUBMITTER: Peraza DA 

PROVIDER: S-EPMC11599228 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature