Despite achievements in the management of cardiovascular disease (CVD) over the last 50 years, CVD remains a primary cause of global morbidity and mortality in both emerging and developed economies. Due to the rising aging population in combination with an increase in cardiometabolic risk factors, the number of individuals affected by CVD is currently on the rise. Therefore, it is of utter importance to develop new strategies aimed at reducing CVD risk and elucidate the molecular mechanisms and important players of CVD, including atherosclerosis and plaque rupture and erosion.
Over the past years, it became evident that a specific CVD, atherosclerosis, is a multifactorial disease that is not only driven by lipids but also by inflammation. Compelling evidence that inflammation and the immune system play a crucial role in atherosclerotic CVD was provided by the landmark Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), performed in 2017. Here it was shown that a monoclonal antibody targeting interleukin-1b (IL-1b), termed Canakinumab, effectively reduced CVD risk and mortality, especially in patients characterized with residual inflammation. This effect was independent of lipid-level lowering. In late 2019, the inflammation hypothesis of atherosclerosis was confirmed in the Colchicine Cardiovascular Outcomes Trial (COLCOT), using the anti-inflammatory agent colchicine in patients with recent myocardial infarction. A follow-up study in 2020 applying colchicine in a randomized trial involving patients with chronic coronary disease (LoDoCo), also showed significant risk reduction. These landmark studies set the stage for identifying drug targets that block atherosclerosis-specific inflammatory pathways as a highly promising strategy to reduce cardiovascular risk.
It is now undisputed that cellular metabolism is important in fueling many pro-atherosclerotic processes in the plethora of cells involved in the disease progression, ranging from endothelial cells to smooth muscle cells, neutrophils, T and B-lymphocytes and monocytes. Current and growing omics studies allow for new insights into cell biology and permit a more holistic and unbiased understanding of mechanisms driving metabolic and immune function. Particularly in the field of cancer biology, rewiring of cellular metabolism has been extensively investigated as a means for cancer cells to obtain sufficient biomass and energy to proliferate, invade, and metastasize. Also, in the field of immunology, significant steps have been undertaken to show that changes in key metabolic programs, are not only important for energy production and biomass but can also govern phenotypic and functional changes in immune cells.
Hence, improving the insight into the role of both vascular- and immuno-metabolism, as important players in CVD and drivers of cardiovascular disease is of utmost importance to be able to offer new therapeutic approaches to combat CVD progression.
This Research Topic aims to provide a series of articles covering all aspects of how vascular- and immuno-metabolism impact cardiovascular disease and how metabolic modulation could be used to alter disease progression. We would particularly encourage submissions that take new omics approaches and their outcomes into consideration, focusing on, but not limited to, the context of atherosclerotic vascular disease, heart failure, obesity, and type II diabetes. We welcome basic research, clinical studies, and reviews. Authors may submit various article types, including Original Research, Brief Research Reports, Reviews, Mini-Reviews, and Systematic Reviews.
Please note: Descriptive studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
Despite achievements in the management of cardiovascular disease (CVD) over the last 50 years, CVD remains a primary cause of global morbidity and mortality in both emerging and developed economies. Due to the rising aging population in combination with an increase in cardiometabolic risk factors, the number of individuals affected by CVD is currently on the rise. Therefore, it is of utter importance to develop new strategies aimed at reducing CVD risk and elucidate the molecular mechanisms and important players of CVD, including atherosclerosis and plaque rupture and erosion.
Over the past years, it became evident that a specific CVD, atherosclerosis, is a multifactorial disease that is not only driven by lipids but also by inflammation. Compelling evidence that inflammation and the immune system play a crucial role in atherosclerotic CVD was provided by the landmark Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), performed in 2017. Here it was shown that a monoclonal antibody targeting interleukin-1b (IL-1b), termed Canakinumab, effectively reduced CVD risk and mortality, especially in patients characterized with residual inflammation. This effect was independent of lipid-level lowering. In late 2019, the inflammation hypothesis of atherosclerosis was confirmed in the Colchicine Cardiovascular Outcomes Trial (COLCOT), using the anti-inflammatory agent colchicine in patients with recent myocardial infarction. A follow-up study in 2020 applying colchicine in a randomized trial involving patients with chronic coronary disease (LoDoCo), also showed significant risk reduction. These landmark studies set the stage for identifying drug targets that block atherosclerosis-specific inflammatory pathways as a highly promising strategy to reduce cardiovascular risk.
It is now undisputed that cellular metabolism is important in fueling many pro-atherosclerotic processes in the plethora of cells involved in the disease progression, ranging from endothelial cells to smooth muscle cells, neutrophils, T and B-lymphocytes and monocytes. Current and growing omics studies allow for new insights into cell biology and permit a more holistic and unbiased understanding of mechanisms driving metabolic and immune function. Particularly in the field of cancer biology, rewiring of cellular metabolism has been extensively investigated as a means for cancer cells to obtain sufficient biomass and energy to proliferate, invade, and metastasize. Also, in the field of immunology, significant steps have been undertaken to show that changes in key metabolic programs, are not only important for energy production and biomass but can also govern phenotypic and functional changes in immune cells.
Hence, improving the insight into the role of both vascular- and immuno-metabolism, as important players in CVD and drivers of cardiovascular disease is of utmost importance to be able to offer new therapeutic approaches to combat CVD progression.
This Research Topic aims to provide a series of articles covering all aspects of how vascular- and immuno-metabolism impact cardiovascular disease and how metabolic modulation could be used to alter disease progression. We would particularly encourage submissions that take new omics approaches and their outcomes into consideration, focusing on, but not limited to, the context of atherosclerotic vascular disease, heart failure, obesity, and type II diabetes. We welcome basic research, clinical studies, and reviews. Authors may submit various article types, including Original Research, Brief Research Reports, Reviews, Mini-Reviews, and Systematic Reviews.
Please note: Descriptive studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
