Table 5 Rat retinal miRs showing higher connectivity in the large gene networks associated with early and late post-IR injury periods along with their reported activities in other systems and relevant citations

Rno-miR-495

Early (24 h)

inhibition of miR-495 increased neovascularization and recovery of blood flow after cardiac ischemia in mice

[60]

Rno-miR-214

miR-214 protected the mouse heart from ischemic injury by controlling Ca²⁺ overload and cell death

[61]

Rno-miR-298

miR-298 was up-regulated in brain and blood after ischemic stroke

[62]

Rno-miR-206

miR-206 was significantly deregulated during the conditions of unfolded protein response in H9c2 rat cardiomyoblasts

[79]

Rno-miR-221

miR-221 was suggested as a biomarker for cerebrovascular disease. Stroke patients and atherosclerosis subjects showed significantly lower miR-221 serum levels than healthy controls

[80]

Rno-miR-873

Late (7d)

miR-873 was up-regulated after onset of focal cerebral ischemia in mice

[63]

Rno-miR-223

miR-223 targeted glutamate receptors in mice brain. Overexpression of miR-223 decreased the levels of GluR2 and NR2B, inhibited NMDA-induced calcium influx in hippocampal neurons, and protected the brain from neuronal cell death following transient global ischemia and excitotoxic injury

[64]

Rno-miR-185

miR-185 has been associated with inflammatory responses during brain ischemic stroke in mice and may provide underlying target for prevention and treatment of stroke

[65]

Rno-miR-329

Inhibition of miR-329 increased neovascularization and blood flow recovery after ischemia in mice subjected to double femoral artery ligation

[60]

Rno-miR-138

hypoxia-induced miR-138 is an essential mediator of endothelial cell dysfunction via targeting S100A1 Ca²⁺ sensor

[81]