Background. Neovascularization, i.e. angiogenesis and arteriogenesis is a multifactorial process. As microRNAs can regulate expression of up to several hundred target genes, we set out to identify microRNAs that target genes in all pathways of neovascularization. Using www.targetscan.org, we performed a reverse target prediction on a set of 197 genes involved in neovascularization. We found enrichment of binding sites for 27 miRs in a single microRNA gene cluster. MicroArray analyses showed that 14q32 microRNAs were down-regulated during neovascularization in mice subjected to single femoral artery ligation. Methods and Results. Novel microRNA-inhibitors, Gene Silencing Oligonucleotides (GSOs), were used to inhibit four 14q32 microRNAs, miR-487b, miR-494, miR-329 and miR-495 one day prior to double femoral artery ligation. Blood flow recovery was followed by Laser Doppler Perfusion Imaging. All 4 GSOs clearly improved blood flow recovery after ischemia. Mice treated with GSO-495 or GSO-329 showed increased perfusion already after 3 days (30% perfusion vs. 15% in control) and those treated with GSO-329 showed a remarkable full recovery of perfusion after 7 days (vs. 60% in control). Increased collateral artery diameters (arteriogenesis) were observed in adductor muscles of GSO-treated mice, as well as increased capillary densities (angiogenesis) in the ischemic soleus muscle. In vitro, treatment with GSO-329, GSO-495 and GSO-487 led to increased arterial endothelial cell activation whereas treatment with GSO-494 led to increased arterial fibroblast proliferation. Conclusions. Inhibition of 14q32 miRs leads to drastic increases in post-ischemic blood flow recovery in vivo and may offer an alternative to growth factors in therapeutic neovascularization.