title: LDL-cholesterol versus HDL-cholesterol in the atherosclerotic plaque: inflammatory resolution versus thrombotic chaos.
abstract: Atherosclerosis is a complex disease in which many processes contribute to lesion development. Yet, it is well accepted that high serum levels of low-density lipoproteins (LDL) play a main role in the initiation and progression of atherosclerosis. Despite currently available optimal LDL-lowering therapies, a worrisome number of clinical events still occur. The protective effect of high-density lipoproteins (HDL) in atherosclerosis, either by suppressing vascular-LDL accumulation, inflammation, oxidation, endothelial damage, and thrombosis, has supported the need of the use of HDL-raising therapies to address this residual risk. Results obtained in some studies, however, have shown that HDL quality, rather than quantity, should be the target of future pharmacological therapies. Here, we will first explore the mechanism by which excess LDL is fundamental in the development of atherosclerosis and its thrombotic complications, behaving as a factor that introduces chaos in the vascular wall. Afterwards, we will explore how functional HDL, through various cellular and molecular mechanisms, facilitates the resolution of this vascular chaos by suppression of atherosclerosis progression and induction of regression.
authors.affiliation: Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau and CIBEROBN-Pathophysiology of Obesity and Nutrition, Barcelona, Spain.|Cardiovascular Research Chair, Universitat Autònoma de Barcelona, Barcelona, Spain.
authors.forename: Lina
authors.initials: L
authors.lastname: Badimon
authors.affiliation: Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau and CIBEROBN-Pathophysiology of Obesity and Nutrition, Barcelona, Spain.
authors.forename: Gemma
authors.initials: G
authors.lastname: Vilahur
mesh_terms: D050197:Atherosclerosis / Q000097:blood / Q000209:etiology / Q000473:pathology; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000209:etiology; D008955:Models, Cardiovascular; D032389:Myocytes, Smooth Muscle / Q000502:physiology; D058226:Plaque, Atherosclerotic / Q000097:blood* / Q000209:etiology* / Q000473:pathology; D012307:Risk Factors; D013927:Thrombosis / Q000209:etiology
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL