The iterative lipid impact on inflammation in atherosclerosis.
Curr Opin Lipidol
; 32(5): 286-292, 2021 10 01.
Article
en En
| MEDLINE
| ID: mdl-34392272
ABSTRACT
PURPOSE OF REVIEW Lipid-mediated atherogenesis is hallmarked by a chronic inflammatory state. Low-density lipoprotein cholesterol (LDL-C), triglyceride rich lipoproteins (TRLs), and lipoprotein(a) [Lp(a)] are causally related to atherosclerosis. Within the paradigm of endothelial activation and subendothelial lipid deposition, these lipoproteins induce numerous pro-inflammatory pathways. In this review, we will outline the effects of lipoproteins on systemic inflammatory pathways in atherosclerosis. RECENT FINDINGS:
Apolipoprotein B-containing lipoproteins exert a variety of pro-inflammatory effects, ranging from the local artery to systemic immune cell activation. LDL-C, TRLs, and Lp(a) induce endothelial dysfunction with concomitant activation of circulating monocytes through enhanced lipid accumulation. The process of trained immunity of the innate immune system, predominantly induced by LDL-C particles, hallmarks the propagation of the low-grade inflammatory response. In concert, bone marrow activation induces myeloid skewing, further contributing to immune cell mobilization and plaque progression.SUMMARY:
Lipoproteins and inflammation are intertwined in atherogenesis. Elucidating the inflammatory pathways will provide new opportunities for therapeutic agents.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Aterosclerosis
Límite:
Humans
Idioma:
En
Revista:
Curr Opin Lipidol
Asunto de la revista:
BIOQUIMICA
Año:
2021
Tipo del documento:
Article