Journal
CELLS
Volume 10, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/cells10112808
Keywords
Racs; atherosclerosis; statins; macrophage; inflammation; calcification
Categories
Funding
- NIH NHLBI
- Institutional Development Award (IDeA) from NIH NIGMS
- A CSRD Merit
- [R01HL139795]
- [P20GM103652]
- [1I01CX002231]
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Coronary artery disease caused by atherosclerosis is a major global cause of morbidity and mortality, with inflammation mediated by immune signaling mechanisms playing a key role. Targeting hypercholesterolemia is a critical strategy in current treatments for atherosclerotic vascular disease, and future directions may involve regulating immune signaling pathways.
Coronary artery disease caused by atherosclerosis is a major cause of morbidity and mortality around the world. Data from preclinical and clinical studies support the belief that atherosclerosis is an inflammatory disease that is mediated by innate and adaptive immune signaling mechanisms. This review sought to highlight the role of Rac-mediated inflammatory signaling in the mechanisms driving atherosclerotic calcification. In addition, current clinical treatment strategies that are related to targeting hypercholesterolemia as a critical risk factor for atherosclerotic vascular disease are addressed in relation to the effects on Rac immune signaling and the implications for the future of targeting immune responses in the treatment of calcific atherosclerosis.
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