mouse hearts; left ventricle heart tissue; LV tissue; ischemic myocardium; injured myocardium; myocardium
RAW 264.7; RAW264.7; HL-1
other disease animal model
immune regulation (promotes); macrophage polarization (promotes); apoptosis (inhibits); angiogenesis (promotes); inflammation (inhibits); ceRNA regulation (promotes); other pathway/process (promotes)
RT-qPCR; Clinical Sample Validation; RNA Pull-Down; Transfection; Flow Cytometry(Non-apoptosis/cycle); IHC (Immunohistochemistry); IF (Immunofluorescence); TUNEL; In Vivo Animal Model; Bioinformatics Analysis
Potential anti-inflammatory therapeutic regulator to improve cardiac repair and post-MI cardiac function.
In this mouse myocardial infarction study, circ-cdr1as was downregulated in early post-MI hearts, particularly in macrophages and cardiomyocytes. Overexpression of circ-cdr1as promoted anti-inflammatory M2-like macrophage polarization, reduced cardiomyocyte apoptosis and infarct size, enhanced vascularization, and improved cardiac function. Mechanistically, circ-cdr1as sponged miR-7 to relieve repression of Klf4/KLF4, forming a circ-cdr1as/miR-7/Klf4 immune-regulatory axis.
0.7113
Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.
biological research