NIH R01 · 2024
The function of Runx1 in cardiac fibroblasts and post-myocardial infarction healing
Project Summary Myocardial infarction (MI) induces the massive death of cardiomyocytes. Quiescent cardiac fibroblasts (CFs) are rapidly activated after MI. They proliferate and differentiate into cardiac myofibroblasts (CMFs), mediating cardiac fibrosis. We recently found that in more stabilized infarct scar CMFs further differentiate into matrifibrocytes, a state resembling partially differentiated chondrocytes, which indicated an advanced level of fibrosis. The post-MI fibrotic response in the heart stabilizes the infarcted myocardium, which may prevent cardiac rupture but also reduce ventricle wall compliance and conductivity, and even interfere with regeneration efforts. Understanding…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.