Why the study?
Does activation of PPAR-α by fibrates contribute to the regression of atherosclerotic plaque and reduction of cardiometabolic risk?
Does activation of PPAR-α by fibrates contribute to the regression of atherosclerotic plaque and reduction of cardiometabolic risk?
PPAR-α activation by fibrates plays a significant role in atherogenesis by modulating lipid metabolism and inflammation, potentially reducing cardiometabolic risk.
Supports mechanistic role for fibrates in atherogenesis; leaves open clinical translation to plaque regression and risk reduction.
Peroxisome proliferator receptors alpha (PPAR-α) and their role in atherogenesis has a great practical significance, since there are drugs that can enhance the activity of these receptors. Activation of PPAR-α by fibrates is known to lead to both significant reduction of serum triglyceride levels by activation of lipoprotein lipase, and to the increase of synthesis of the main apolipoproteins within high-density lipoproteins (HDL), contributing to the reverse transport of cholesterol from chylomicrons and very low-density lipoproteins to the liver. Besides, PPAR-α increase the capture of HDL by liver. PPAR-α also participate in the regulation of inflammation, expression of adhesive molecules, production of chemotactic factors, as well as inhibit the proliferation of smooth muscle cells and activity of fibroblasts. These data suggest that PPAR-α are directly involved in the processes of atherogenesis, and their activation may contribute to the regression of atherosclerotic plaque and significant reduction of cardiometabolic risk.
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Krasilnikova et al. (2012) studied this question.
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