The role of colchicine in reducing cardiac remodeling process in no revas group
TGF-β1, cardiac hypertrophy
PROLIFERATION, HEART FAILURE, MYOCARDIAL INFARCTION, CARDIAC HYPERTROPHY
MMP-9, NOX2, and TGF-β1 analysis in OMT + Colchicine group is significantly different and lower than OMT + Placebo group: MMP9 (Day-1: p = 0.001; Day-5: p = 0.022), NOX2 (Day-1: p = 0.02; Day-5: p = 0.026), and TGF-β (Day-1: p = 0.00; Day-5: p = 0.00). The results may suggest the role of colchicine to regulate the biomarkers. Despite the molecular mechanisms, myocardial infarction also affects the microtubules of cardiomyocytes. During the transition from cardiac remodeling and cardiac hypertrophy to heart failure, several structural modifications in cardiomyocytes affect both systolic and diastolic activity. A doubled microtubule network has been identified as a possible reason for poor performance [When there is an increase in ROS generation, mediated by NOX2, microtubule proliferation occurs in myocytes, and vice versa [Colchicine improves right ventricular function and t-tubule architecture, whereas reducing microtubule density and junctophilin-2 expression. This study is supported by the molecular docking study by Suryono et al. that demonstrates colchicine may decrease several biomarkers like MMP-9, NOX2, and TGF-β1 [
Colchicine mechanism to inhibit ventricle remodeling process