Cardiovascular diseases (CVD) represent the primary cause of morbidity and mortality in industrialized countries. With the largest share of inpatient and pharmaceutical spending, CVD accounts for more than 10% of overall costs in healthcare.
Low-grade chronic inflammation mediated by cells of the innate and adaptive immune system has long been recognized to drive development and progression of CVD. A dysfunctional interplay of pro- and anti-inflammatory immune cells in the vessel wall as well as an altered expression and metabolism profile of immune cells leads to restructuring of the vasculature, thereby driving disease progression. Accordingly, immunological processes are an attractive therapeutic target for improving the outcome of CVD. As of today, measures for prevention of cardiovascular events established in clinical practice primarily focus on lifestyle changes, lipid lowering, angiotensin inhibition, platelet inhibition and anticoagulation. However, preclinical studies and few clinical randomized trials, such as CANTOS, demonstrate that modulating inflammation reduces progression of CVD and prevents cardiovascular events. The development of new molecular methods and gene therapy approaches provide useful tools for modulating interactions of endothelial cells with the immune system. Recent strategies such as suppression of pro-inflammatory mediators, selective expansion of anti-inflammatory cell subtypes, immunization against atherosclerotic antigens or use of checkpoint inhibitors have been identified as promising therapeutic targets for the prevention or delay of CVD and its associated complications. A deeper mechanistic understanding of innate and adaptive immunity in the pathophysiology of CVD could pave the way for the development of novel therapies to reduce morbidity and mortality of CVD.
This article collection aims to define compelling strategies targeting innate or adaptive immunity for improving outcomes of CVD. We welcome state-of-the art reviews and original manuscripts, basic and clinical research, and mechanistic and therapeutic approaches.
Topic Editor Jan Larmann received financial support from Mitsubishi Chemical Europe and Philips Medizinsysteme. Topic Editor L. Christian Napp received financial support from Abbott, Abiomed, Bayer, Berlin Cures, Cytosorbents, and MHH intramural funds. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Cardiovascular diseases (CVD) represent the primary cause of morbidity and mortality in industrialized countries. With the largest share of inpatient and pharmaceutical spending, CVD accounts for more than 10% of overall costs in healthcare.
Low-grade chronic inflammation mediated by cells of the innate and adaptive immune system has long been recognized to drive development and progression of CVD. A dysfunctional interplay of pro- and anti-inflammatory immune cells in the vessel wall as well as an altered expression and metabolism profile of immune cells leads to restructuring of the vasculature, thereby driving disease progression. Accordingly, immunological processes are an attractive therapeutic target for improving the outcome of CVD. As of today, measures for prevention of cardiovascular events established in clinical practice primarily focus on lifestyle changes, lipid lowering, angiotensin inhibition, platelet inhibition and anticoagulation. However, preclinical studies and few clinical randomized trials, such as CANTOS, demonstrate that modulating inflammation reduces progression of CVD and prevents cardiovascular events. The development of new molecular methods and gene therapy approaches provide useful tools for modulating interactions of endothelial cells with the immune system. Recent strategies such as suppression of pro-inflammatory mediators, selective expansion of anti-inflammatory cell subtypes, immunization against atherosclerotic antigens or use of checkpoint inhibitors have been identified as promising therapeutic targets for the prevention or delay of CVD and its associated complications. A deeper mechanistic understanding of innate and adaptive immunity in the pathophysiology of CVD could pave the way for the development of novel therapies to reduce morbidity and mortality of CVD.
This article collection aims to define compelling strategies targeting innate or adaptive immunity for improving outcomes of CVD. We welcome state-of-the art reviews and original manuscripts, basic and clinical research, and mechanistic and therapeutic approaches.
Topic Editor Jan Larmann received financial support from Mitsubishi Chemical Europe and Philips Medizinsysteme. Topic Editor L. Christian Napp received financial support from Abbott, Abiomed, Bayer, Berlin Cures, Cytosorbents, and MHH intramural funds. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
