Nitric Oxide, Oxidative Stress, and Interplay in Diabetic Endothelial Dysfunction

Table 2

Modulated miRNAs in diabetic endothelial dysfunction and oxidative stress.

ROS; source/disease	miRNAs	Tissue/organ	Source	Target	Functions	References
	Upregulated
H2O2	miR-200c, miR-141,; miR-200a, miR-200b, and; miR-429	ECs, myoblasts	Human	ZEB1	Apoptosis, senescence	[120]
Diabetes	miR-200c, miR-200b, and; miR-429	VSMCs	Mouse	ZEB1	Inflammation	[118]
NO	miR-200c, miR-200a,; miR-200b, and miR-429	mES	Mouse	ZEB2	Mesendoderm and cardiovascular differentiation	[121]
Hypoxia	miR-210	ECs	Human	EFNA3	Angiogenesis	[125]
Diabetes	miR-210	Failing heart	Human			[127]
Diabetes	miR-125	VSMCs	Mouse	Suv39h1	Inflammation	[122]
	Downregulated
Diabetes	miR-27b	BMACs	Human/mouse	Sema6A, p66^shc, and TSP-1	ROS production; angiogenesis impairment	[124]

BMACs: bone marrow-derived angiogenic cells, ECs: endothelial cells, EFNA3: Ephrin A3, H₂O₂: hydrogen peroxide, mES: mouse embryonic stem, NO: nitric oxide, p66^Shc: p66 isoform of ShcA protein, ROS: reactive oxygen species, Sema6A: semaphorin 6A, Suv39h1: suppressor of variegation 3-9 homolog 1 (Drosophila), TSP-1: thrombospondin-1, VSMCs: vascular smooth muscle cells, ZEB1: zinc finger E-box binding homeobox 1, and ZEB2: zinc finger E-box binding homeobox 2.