This article deals with the role of c-reactive protein (CRP) in the development of atherosclerosis and its treatment. CRP has a predictive value in ischemic heart disease, restenosis, coronary artery disease, aortic atherosclerosis, and cerebrovascular disease. This article deals with the synthesis and mechanism of CRP-induced atherosclerosis and its treatment. CRP increases the formation of numerous atherogenic biomolecules such as reactive oxygen species (ROS), cytokines (interleukin [IL]-1β and IL-6), cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, activated complement C5, monocyte colony-stimulating factor, and numerous growth factors [insulin-like growth factor, platelet-derived growth factor, and transforming growth factor-β]). ROS mildly oxidizes low-density lipoprotein (LDL)-cholesterol to form minimally modified LDL which is further oxidized to form oxidized LDL. The above atherogenic biomolecules are involved in the development of atherosclerosis and has been described in detail in the text. This paper also deals with the treatment modalities for CRP-induced atherosclerosis which includes lipid-lowering drugs, antihypertensive drugs, antioxidants, aspirin, antidiabetic drugs, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, regular physical activity, weight reduction, and stoppage of cigarette smoking. In conclusion, CRP induces atherosclerosis through increases in atherogenic biomolecules and the treatment modalities would prevent, regress, and slow the progression of CRP-induced atherosclerosis.

Article published online:
18 July 2024

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