**4. Conclusions**

The remodeling of pre-existing arteriolar collaterals during arteriogenesis is a complex process requiring the highly-coordinated interplay of different leukocytes to promote endothelial and smooth muscle cell proliferation and to ultimately establish perfusion. eRNA has been demonstrated to translate fluid shear stress into endothelial activation during arteriogenesis, further stimulating vWF release, PNA formation, mast cell degranulation and leukocyte recruitment, culminating in the beneficial process of arteriogenesis to promote perfusion recovery. In contrast to the beneficial role of eRNA in arteriogenesis, eRNA has been formerly established as a damaging or pathological factor in a variety of cardiovascular diseases based upon its modulation of endothelial cell and leukocyte function, whereby administration of RNase1 was demonstrated to serve as a tissue- and vessel-protective regimen. It remains to be established which particular molecular interactions and binding partners as well as which putative cellular receptors for eRNA appear to be responsible for its either adverse or beneficial functions in the cardiovascular system.

**Author Contributions:** Writing—Original Draft Preparation, A.-K.K. and A.B.; Writing—Review & Editing, S.F., K.T.P. and E.D.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflict of interest.
