Table 3.

CAD-related miRNAs whose function has been assessed in macrophages/ monocytes.

microRNA	Samples	Expression pattern	Assessed cell lines	Gene/protein interactions	Signaling pathway	Function	References
miR-23a	Blood samples (PBMCs) from 104 CAD patients and 50 control subjects	Up-regulated	PBMCs	TRF2	–	Contributes to telomere shortening and cellular senescence through targeting TRF2	(33)
miR-4306	Blood samples (platelet-derived microparticles) form CAD patients (24 AMI patients and 16 patients with stable angina pectoris) and 20 controls, C57BL/6 mice	Down-regulated	Primary human monocyte-derived macrophages	–	VEGFA/ERK1/2/NF-κB signaling pathways	Suppresses migration of HMDMs by regulating VEGFA/ERK1/2/NF-κB signaling pathways	(32)
miR-3614	epicardial adipose tissue from 30 CAD patients and 30 controls	Down-regulated	THP-1 (monocyte)	TRAF6	–	Its overexpression regulated inflammatory responses by targeting TRAF6	(34)
miR-124	Plasma samples from 40 patients with CAD and 40 non-CAD individuals, ApoE−/− C57B/L6J mice	Down-regulated	RAW264.7 (mouse macrophage cell line)	p38	MAPK signaling pathway	Its overexpression decreased expression of pro-inflammatory cytokines and enhanced expression of anti-inflammatory cytokines	(36)
miR-16	Blood samples (plasma and PBMCs) from 40 patients with CAD and 40 non-CAD patients, 22 ApoE−/− mice	Down-regulated	Peripheral blood mononuclear cells	PDCD4	–	Its overexpression Suppresses atherosclerotic plaque formation and proinflammatory factors secretion and promotes release of anti-inflammatory factors	(35)
miR-21	Circulating monocytes from CAD patients and non-CAD patients, apoE−/− mice and miR-21−/−apoE−/− mice	Up-regulated	Bone-marrow-derived macrophage	Dusp-8	–	Its knockout in mice caused decreased atherosclerotic lesions and smooth muscle cells in aorta also reduced macrophage migration and macrophage-endothelium interaction.	(37)