Anti-inflammatory Action of Statins in Cardiovascular Disease: the Role of Inflammasome and Toll-Like Receptor Pathways.
Animals
Anti-Inflammatory Agents
/ therapeutic use
Cardiovascular Diseases
/ drug therapy
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ therapeutic use
Inflammasomes
/ metabolism
Interleukin-18
/ metabolism
Interleukin-1beta
/ metabolism
NF-kappa B
/ metabolism
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Signal Transduction
Toll-Like Receptors
/ metabolism
Atherosclerosis
Cardiovascular disease
Inflammasome
NLRP3
Statins
TLR2
TLR4
Journal
Clinical reviews in allergy & immunology
ISSN: 1559-0267
Titre abrégé: Clin Rev Allergy Immunol
Pays: United States
ID NLM: 9504368
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
pubmed:
8
5
2020
medline:
3
11
2021
entrez:
8
5
2020
Statut:
ppublish
Résumé
Atherosclerosis is one type of cardiovascular disease (CVD) in which activation of the NLRP3 inflammasome and toll-like receptor (TLR) pathways is implicated. One of the most effective treatments for atherosclerosis is the use of statin medications. Recent studies have indicated that statins, in addition to their lipid-lowering effects, exert inhibitory and/or stimulatory effects on the NLRP3 inflammasome and TLRs. Some of the statins lead to activation of the inflammasome and subsequently cause secretion of IL-1β and IL-18. Thus, these actions may further aggravate the disease. On the other hand, some statins cause inhibition of the inflammasome or TLRs and along with lipid-lowering, help to improve the disease by reducing inflammation. In this article, we discuss these contradictory studies and the mechanisms of action of statins on the NLRP3 inflammasome and TLR pathways. The dose-dependent effects of statins on the NLRP3 complex are related to their chemistry, pharmacokinetic properties, and danger signals. Lipophilic statins have more pleiotropic effects on the NLRP3 complex in comparison to hydrophilic statins. Statins can suppress TLR4/MyD88/NF-ĸB signaling and cause an immune response shift to an anti-inflammatory response. Furthermore, statins inhibit the NF-ĸB pathway by decreasing the expression of TLRs 2 and 4. Statins are cost-effective drugs, which should have a continued future in the treatment of atherosclerosis due to both their immune-modulating and lipid-lowering effects.
Identifiants
pubmed: 32378144
doi: 10.1007/s12016-020-08791-9
pii: 10.1007/s12016-020-08791-9
pmc: PMC7985098
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Inflammasomes
0
Interleukin-18
0
Interleukin-1beta
0
NF-kappa B
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Toll-Like Receptors
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
175-199Références
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