Table. .

Speculation of the Role of miRNAs, Phase They Should Be Administered, Their Blockade/Overexpression And Reduction in HSK Lesion Severity (Mild +, Moderate ++, Severe +++)

Steps	miRNAs	Action	Preclinical (0–6 d p.i.)/Clinical Phase (7–12 d p.i.) Administration	Reduction in HSK Lesions/CV (overexpression or blockade)
Corneal neovascularization
VEGF signaling	miR-132	Promotes VEGF signaling	Clinical phase	Blockade (++)
MMP-9	miR-885-5p, miR-491-5p, miR-212	Negatively regulates MMP-9 activity	Preclinical phase	Overexpression (+)
Inflammation
IL-17–induced inflammation	miR-23b	Negatively regulates NFkB and IL-17 activity	Preclinical phase	Overexpression (++)
T cell–mediated damage	miR-155	Generation of Th1 and Th17 cells	Clinical phase	Blockade (++)
	miR-29	IFN-γ production by Th1 cells	Preclinical phase	Blockade (+)
	miR-326 and miR-309	Generation of Th17 cells	Preclinical phase	Blockade (+)
	miR-17 and miR-20a	Inhibits T cell activation	Preclinical phase	Blockade (+)
	miR-182	T cell proliferation	Preclinical phase	Blockade (+)
Resolution
T cell responses	miR-146a	Resolution of T cell–mediated damage	Clinical phase	Overexpression (+++)
		Necessary for Tregs to control Th1 responses
		Regulates NFkB and proinflammatory cytokines
IL-10 production	miR-21 and miR-208a	Induces IL-10 production	Clinical phase	Overexpression (++)
Neutrophil recruitment	miR-146b	Lowers IL-8 and RANTES	Clinical phase	Overexpression (+)
Lipid mediator switch	miR-292-2	Lowers leukotrienes and turns on SPM	Clinical phase	Overexpression (++)
Tregs	miR-10a	Stabilizes tregs	Clinical phase	Overexpression (+)