Atherosclerosis represents the main culprit of cardiovascular diseases and develops from an unbalanced lipid metabolism coupled to inflammation. Parallel to local infiltration of immune cells, such as monocyte-derived macrophages and lymphocytes, systemic changes in the number, proportion and function of immune cells have been reported in patients with cardiovascular diseases (CVD). Recent clinical trials with anti-inflammatory therapies (CANTOS, COLCOT and LoDoCo2) have contributed to demonstrate the causality of the association between the CVD and systemic immuno-inflammatory responses, suggesting that the activation of immune response is not merely a bystander of lipid overload, but instead is actively involved in disease progression. Furthermore, emerging evidence show that the pro-inflammatory activation of immune cells occurs already at the level of hematopoietic precursors even in the bone marrow by mechanisms of functional priming and/or clonal hematopoiesis, that were shown to increase the risk of atherosclerotic cardiovascular disease.
Lipid lowering therapy represents the pillar for decreasing circulating LDL-C levels; however, a proportion of patients still experience a cardiovascular risk that is often associated to the inflammatory burden. This scenario claims at investigating novel strategy to correct the unwanted immune-inflammatory response by understanding the molecular mechanisms of immune cell failure in the context of atherosclerosis-driven inflammation. This approach would offer a tailored strategy to target immune cells in the context of atherosclerotic plaque, limiting systemic effect on immune response under different circumstances, such as infections.
While lipid-lowering agents have demonstrated to possess a several immunomodulatory functions by improving systemic lipid profile, understanding how immune cells integrate cellular function with metabolic and energetic circuits is increasingly being recognized. Therefore, the identification of metabolic “checkpoints” that couple the reprogram of energetic machinery with immune cell functionality is becoming attractive as an innovative way to target the inflammatory response associated to atherosclerosis.
This article collection aims at gathering state-of-the-art knowledge about the functional and metabolic adaptations of immune cells in the context of atherosclerosis and cardiovascular/metabolic disorders with the scope of identifying potential innovative strategies to target immune cell function. We welcome cutting edge reviews and original manuscripts, basic and clinical research from any groups working on the crosstalk between cardiovascular immunology and metabolism.
Specific topics are listed below but are not limited to:
1) Macrophages role and metabolism in atherosclerosis.
2) Hematopoiesis in CVD.
3) Targeting lymphocytes in atherosclerosis.
4) Metabolic adaptations of cells within the atherosclerotic plaque.
5) Myeloid cells impairment in CVD.
Atherosclerosis represents the main culprit of cardiovascular diseases and develops from an unbalanced lipid metabolism coupled to inflammation. Parallel to local infiltration of immune cells, such as monocyte-derived macrophages and lymphocytes, systemic changes in the number, proportion and function of immune cells have been reported in patients with cardiovascular diseases (CVD). Recent clinical trials with anti-inflammatory therapies (CANTOS, COLCOT and LoDoCo2) have contributed to demonstrate the causality of the association between the CVD and systemic immuno-inflammatory responses, suggesting that the activation of immune response is not merely a bystander of lipid overload, but instead is actively involved in disease progression. Furthermore, emerging evidence show that the pro-inflammatory activation of immune cells occurs already at the level of hematopoietic precursors even in the bone marrow by mechanisms of functional priming and/or clonal hematopoiesis, that were shown to increase the risk of atherosclerotic cardiovascular disease.
Lipid lowering therapy represents the pillar for decreasing circulating LDL-C levels; however, a proportion of patients still experience a cardiovascular risk that is often associated to the inflammatory burden. This scenario claims at investigating novel strategy to correct the unwanted immune-inflammatory response by understanding the molecular mechanisms of immune cell failure in the context of atherosclerosis-driven inflammation. This approach would offer a tailored strategy to target immune cells in the context of atherosclerotic plaque, limiting systemic effect on immune response under different circumstances, such as infections.
While lipid-lowering agents have demonstrated to possess a several immunomodulatory functions by improving systemic lipid profile, understanding how immune cells integrate cellular function with metabolic and energetic circuits is increasingly being recognized. Therefore, the identification of metabolic “checkpoints” that couple the reprogram of energetic machinery with immune cell functionality is becoming attractive as an innovative way to target the inflammatory response associated to atherosclerosis.
This article collection aims at gathering state-of-the-art knowledge about the functional and metabolic adaptations of immune cells in the context of atherosclerosis and cardiovascular/metabolic disorders with the scope of identifying potential innovative strategies to target immune cell function. We welcome cutting edge reviews and original manuscripts, basic and clinical research from any groups working on the crosstalk between cardiovascular immunology and metabolism.
Specific topics are listed below but are not limited to:
1) Macrophages role and metabolism in atherosclerosis.
2) Hematopoiesis in CVD.
3) Targeting lymphocytes in atherosclerosis.
4) Metabolic adaptations of cells within the atherosclerotic plaque.
5) Myeloid cells impairment in CVD.
