Cholesterol efflux pathways, inflammation, and atherosclerosis
| Autor: | Anouk G. Groenen, Benedek Halmos, Alan R. Tall, Marit Westerterp |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
ET-AL
Inflammasomes Biochemistry chemistry.chemical_compound High-density lipoprotein BINDING CASSETTE TRANSPORTERS Macrophage RNA-Seq Liver X Receptors Foam cell GENE-EXPRESSION 0303 health sciences Chemistry 030302 biochemistry & molecular biology Inflammasome lipids (amino acids peptides and proteins) Single-Cell Analysis medicine.symptom medicine.drug medicine.medical_specialty Biological Transport Active Inflammation high-density lipoprotein 03 medical and health sciences LIPID-METABOLISM Internal medicine medicine Animals Humans CORONARY-HEART-DISEASE Liver X receptor Molecular Biology Cell Proliferation 030304 developmental biology HDL CHOLESTEROL Cholesterol Cholesterol HDL Mendelian Randomization Analysis Hematopoietic Stem Cells Atherosclerosis cardiovascular diseases REVEALS NONFOAMY RATHER Endocrinology Gene Expression Regulation inflammation ACCELERATES ATHEROSCLEROSIS HIGH-DENSITY-LIPOPROTEIN cholesterol efflux FOAMY PLAQUE MACROPHAGES Lipoprotein |
| Zdroj: | Critical reviews in biochemistry and molecular biology. 56(4):426-439 |
| ISSN: | 1040-9238 |
| Popis: | Plasma levels of high-density lipoprotein (HDL) inversely correlate with the incidence of cardiovascular diseases (CVD). The causal relationship between plasma HDL-cholesterol levels and CVD has been called into question by Mendelian randomization studies and the majority of clinical trials not showing any benefit of plasma HDL-cholesterol raising drugs on CVD. Nonetheless, recent Mendelian randomization studies including an increased number of CVD cases compared to earlier studies have confirmed that HDL-cholesterol levels and CVD are causally linked. Moreover, several studies in large population cohorts have shown that the cholesterol efflux capacity of HDL inversely correlates with CVD. Cholesterol efflux pathways exert anti-inflammatory and anti-atherogenic effects by suppressing proliferation of hematopoietic stem and progenitor cells, and inflammation and inflammasome activation in macrophages. Cholesterol efflux pathways also suppress the accumulation of cholesteryl esters in macrophages, i.e. macrophage foam cell formation. Recent single-cell RNASeq studies on atherosclerotic plaques have suggested that macrophage foam cells have lower expression of inflammatory genes than non-foam cells, probably reflecting liver X receptor activation, upregulation of ATP Binding Cassette A1 and G1 cholesterol transporters and suppression of inflammation. However, when these pathways are defective lesional foam cells may become pro-inflammatory. |
| Databáze: | OpenAIRE |
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