Lipid metabolism and atherosclerosis pathways (N/A)

Lipid metabolism and atherosclerosis pathways encompass multiple molecular targets involved in the development and progression of atherosclerosis. Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids in arterial walls, leading to plaque formation[1][5]. Key components of these pathways include receptors like scavenger receptors, ALK1, and PPARs that regulate lipid uptake, transport, and metabolism. The transcytosis of LDL across arterial endothelium is considered a rate-limiting step in atherosclerosis initiation and progression[3]. ALK1 has been identified as a significant mediator of LDL transcytosis, with inhibition reducing lesion area and lipid deposition by approximately 50% in animal models[3]. Peroxisome proliferator-activated receptors (PPARs) are important therapeutic targets for diabetes, dyslipidemia, and atherosclerosis due to their role in lipid metabolism[1]. Other potential targets include endoglin receptor, squalene synthase, and thyroid hormone analogues[1]. The pathways involve complex interactions between lipid metabolism and inflammatory processes. Elevated plasma levels of atherogenic lipoproteins increase their entry into the subendothelium, while particle size (<70 nm) determines their ability to cross the endothelium and become retained within artery walls[4]. Inflammation participates in all phases of atherosclerosis, with inflammatory cytokines causing intracellular lipid accumulation[5]. Recent research has highlighted the role of non-coding RNAs (microRNAs and long non-coding RNAs) as potential therapeutic targets for atherosclerosis treatment[5]. These molecules regulate HDL biogenesis, cholesterol efflux, lipid metabolism, smooth muscle proliferation, and inflammation control[5]. Therapeutic approaches targeting these pathways aim to reduce LDL-cholesterol levels, inhibit lipid accumulation, prevent foam cell formation, and control inflammation to halt atherosclerosis progression and reduce cardiovascular risk[4][5].

Other names

Lipid-related atherosclerosis pathwaysAtherogenic pathwaysLipid accumulation and inflammatory pathways in atherosclerosis

Reduction of atherogenic lipoproteins; Anti-inflammatory effects; Inhibition of LDL transcytosis across arterial endothelium; Promotion of cholesterol efflux; Inhibition of foam cell formation; Regulation of HDL biogenesis; Inhibition of scavenger receptor expression