Key result
PPAR nuclear receptors drive context-dependent effects on atherosclerosis by regulating lipids, inflammation, and vascular remodeling.
This review highlights the complex, context-dependent roles of PPARs in atherosclerosis and evaluates their therapeutic potential.
Atherosclerosis, a leading cause of cardiovascular diseases, is a chronic, progressive condition driven by lipid dysregulation, endothelial dysfunction, and immune cell infiltration. The PPAR (peroxisome proliferator-activated receptor) family of nuclear receptors (PPARα, PPARδ, and PPARγ) is a pivotal regulator of glucose and lipid metabolism, inflammation, and vascular homeostasis. Emerging evidence reveals that PPARs exert complex, context-dependent effects on atherosclerosis that varies by tissue and cell type. This review summarizes the functions and molecular mechanisms of PPARs in the development and treatment of atherosclerosis, focusing on their roles in lipid metabolism, inflammation, and vascular remodeling. We also evaluate the therapeutic potential of PPAR-targeted strategies and highlight critical knowledge gaps for future research.
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Wang et al. (2025) conducted a review in Atherosclerosis. PPARs (PPARα, PPARδ, and PPARγ) was evaluated. The PPAR family of nuclear receptors exerts complex, context-dependent effects on atherosclerosis that vary by tissue and cell type, regulating lipid metabolism, inflammation, and vascular remodeling.
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