NIH R01 · 2024
Cell-specific role and therapeutic potential of KCa3.1 in atherosclerosis
Pathogenesis of coronary artery disease is complex, with multiple cell types contributing to lesion size and composition. Acute coronary syndromes are most often associated with rupture of complex, vulnerable plaques that are otherwise clinically benign. The progression to either a relatively benign, stable lesion or a rupture-prone, vulnerable plaque has been linked to key lesion characteristics, i.e. smooth muscle (SM) and collagen content, macrophage infiltration and necrotic core area within the lesion. The objectives of this proposal are to 1) determine the SM-specific role and underlying mechanism(s) by which the intermediate conductance, Ca2+-activated K+ channel, KCa3.1 (encoded by…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.