Summary
Severe inflammatory complications are a potential consequence in patients with predetermined
conditions of infections, pulmonary diseases, or cardiovascular disorders. Notably,
the amplitude of the inflammatory response towards these complications can dictate
the disease progression and outcome. During the recent years, evidence from basic
research as well as from clinical studies has identified self-extracellular nucleic
acids as important players in the crosstalk between immunity and cardiovascular diseases.
These stress- or injury-induced endogenous polymeric macromolecules not only serve
as “alarmins” or “Danger-associated molecular patterns” (DAMPs), but their functional
repertoire goes far beyond such activities in innate immunity. In fact, (patho-) physiological
functions of self-extracellular DNA and RNA are associated and in many cases causally
related to arterial and venous thrombosis, atherosclerosis, ischemia-reperfusion injury
or tumour progression. Yet, the underlying molecular mechanisms are far from being
completely understood. Interestingly enough, however, novel antagonistic approaches
in vitro and in vivo, particularly using natural endonucleases or synthetic nucleic acid binding polymers,
appear to be promising and safe therapeutic options for future studies. The aim of
this review article is to provide an overview of the current state of (patho-) physiological
functions of self-extracellular nucleic acids with special emphasis on their role
as beneficial / alerting or adverse / damaging factors in connection with immune responses,
inflammation, thrombosis, and cardiovascular diseases.
Keywords
Arterial thrombosis - atherothrombosis - bacterial infection - contact phase - immunity