Table 1.

CAD-related miRNAs whose function has been assessed in endothelial cells.

microRNA	Samples	Expression pattern	Assessed cell lines	Gene/protein interactions	Signaling pathway	Function	References
miR-92a-3p	Plasma circulating microvesicles from 41 angiographically excluded CAD patients, 77 patients with stable CAD and 62 patients with acute coronary syndrome	Up-regulated	ECs	THBS1	–	Its knockdown attenuates migration and proliferation of endothelial cells through increasing THBS1 expression	(13)
miR-206	Blood samples from 78 patients with CAD and 65 healthy controls	Up-regulated	EPCs (endothelial progenitor cells)	VEGF	–	Inhibits invasion and cell viability in EPCs can suppress expression of VEGF	(14)
miR-206	Endothelial progenitor cells collected from peripheral blood of 53 CAD patients and 34 healthy controls, Nude mice	Up-regulated	EPCs	PIK3C2α	–	Reduces migration and its knockdown rescued angiogenic and vasculogenic abilities of endothelial progenitor cells	(15)
miR-216a	Blood samples from 176 patients with CAD and 342 age-matched control individuals	Up-regulated	HUVECs	Smad3	–	Promotes monocytes adhesion, endothelial senescence and inflammation through regulating Smad3/IκBα axis	(16)
miR-499	Plasma samples from 216 CAD patients and 90 healthy individuals	Up-regulated	HUVECs	PDCD4	NF-Kβ/TNF-α signaling pathway	Promotes apoptosis rate and decreases survival rate of endothelial cells by reducing expression of PDCD4	(23)
miR-451	Blood samples form 30 patients with coronary heart disease and 30 healthy controls	Up-regulated	HUVECs	VEGFA	PI3K-Akt-mTOR pathway	Suppresses cell proliferation and induces apoptosis in HUVECs by targeting VEGFA	(24)
miR-107	80 specific-pathogen-free (SPF) Kunming mice	Down-regulated	vascular endothelial cells	KRT1	Notch signaling pathway	Its overexpression decreases apoptosis and inflammation so prevents atherosclerosis by targeting KRT1 and activating Notch signaling pathway	(17)
miR-330	Female specific pathogen free (SPF) rats with acute coronary syndrome	Down-regulated	vascular endothelial cells	MAPK8	WNT signaling pathway	Its overexpression inhibits formation of atherosclerotic plaques and promotes proliferation of vascular endothelial cells by targeting MAPK8	(18)
miR-939	Blood samples from 25 CAD patients with poor CCC and 22 CAD patients with sufficient CCC	Down-regulated	HUVECs	γ-catenin	–	Suppresses angiogenesis and abrogates vascular integrity by targeting γ-catenin	(20)
miR-181a-5p miR-181a-3p	Plasma samples from 15 CAD patients and 20 healthy controls, ApoE−/− mice	Down-regulated	HUVECs	TAB2, NEMO	NF-κB signaling pathway	miR-181a-5p and miR-181a-3p overexpression prevents endothelium inflammation and atherosclerosis progression by targeting TAB2 and NEMO, respectively. Also they suppresses expression of adhesion molecule	(21)
miR-376a-3p	Analysis of gene and microRNA expression profile datasets	Down-regulated	HUVECs	NRIP1	–	Its overexpression augmented cell proliferation by targeting NRIP1 in NRIP1	(22)
miR-495	Plasma samples form 30 CAD patients and 30 age and sex matched healthy controls	Down-regulated	HUVECs	CCL2	–	Regulated apoptosis and proliferation of HUVECs by targeting CCL2	(25)
miR-383-3p	30 male Sprague-Dawley (SD) rats with coronary artery atherosclerosis	Down-regulated	Coronary artery endothelial cells	IL1R2	–	Its upregulation reduces inflammatory cytokines expression and apoptosis rate in homocysteine-induced coronary artery endothelial cells by interacting with IL1R2	(19)
miR-218	Serum samples from 104 CAD patients and 101 healthy controls	Down-regulated	cardiac microvascular endothelial cells	–	–	Its upregulation promotes angiogenesis, cell proliferation and migration, enhances apoptosis rate and decreases inflammatory injury to CMECs	(26)