TABLE 1.

ExRNA-counteracting properties of RNase1 as studied in vitro and in preclinical disease models.

Biological system, pathological process	Influence/activity of RNase1	References
Blood coagulation, thrombosis	Destruction of exRNA as cofactor for coagulation proteases; anti-thrombotic	Kannemeier et al., 2007
Vascular hyperpermeability, vasogenic edema formation, stroke	Destruction of exRNA as cofactor for VEGF; vessel-protective	Fischer et al., 2007; Walberer et al., 2009
Inflammation	Destruction of exRNA as cytokine cofactor; anti-inflammatory	Bedenbender and Schmeck, 2020
Tumor growth in xenograft, immuno-compromised model	Destruction of exRNA as triggering factor for promoting tumor cell trafficking; anti-tumorigenic	Fischer et al., 2013
Atherosclerosis, arterial vessel degeneration	Destruction of exRNA as multifunctional cell-damaging factor; anti-atherogenic	Simsekyilmaz et al., 2014
Cardiac ischemia-reperfusion injury, heart failure	Destruction of exRNA as cardiomyocyte-damaging and cytokine-mobilizing factor; anti-cytotoxic, cardio-protective	Cabrera-Fuentes et al., 2014
Experimental heart transplantation	Prolongation of graft survival; tissue-protective	Kleinert et al., 2016
Microbial infection	Prevention of exRNA-mediated bacterial adherence and invasion; anti-microbial	Zakrzewicz et al., 2016
Myocardial infarction	Reduction of cardiac edema and infarct size; cardio-protective	Stieger et al., 2017
Shear stress-mediated induction of arteriogenesis	Reduction of collateral vessel formation; anti-inflammatory	Lasch et al., 2019