Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities.
Journal
Nature reviews. Cardiology
ISSN: 1759-5010
Titre abrégé: Nat Rev Cardiol
Pays: England
ID NLM: 101500075
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
pubmed:
9
3
2019
medline:
21
1
2020
entrez:
9
3
2019
Statut:
ppublish
Résumé
Atherosclerosis is a lipid-driven inflammatory disease of the arterial intima in which the balance of pro-inflammatory and inflammation-resolving mechanisms dictates the final clinical outcome. Intimal infiltration and modification of plasma-derived lipoproteins and their uptake mainly by macrophages, with ensuing formation of lipid-filled foam cells, initiate atherosclerotic lesion formation, and deficient efferocytotic removal of apoptotic cells and foam cells sustains lesion progression. Defective efferocytosis, as a sign of inadequate inflammation resolution, leads to accumulation of secondarily necrotic macrophages and foam cells and the formation of an advanced lesion with a necrotic lipid core, indicative of plaque vulnerability. Resolution of inflammation is mediated by specialized pro-resolving lipid mediators derived from omega-3 fatty acids or arachidonic acid and by relevant proteins and signalling gaseous molecules. One of the major effects of inflammation resolution mediators is phenotypic conversion of pro-inflammatory macrophages into macrophages that suppress inflammation and promote healing. In advanced atherosclerotic lesions, the ratio between specialized pro-resolving mediators and pro-inflammatory lipids (in particular leukotrienes) is strikingly low, providing a molecular explanation for the defective inflammation resolution features of these lesions. In this Review, we discuss the mechanisms of the formation of clinically dangerous atherosclerotic lesions and the potential of pro-resolving mediator therapy to inhibit this process.
Identifiants
pubmed: 30846875
doi: 10.1038/s41569-019-0169-2
pii: 10.1038/s41569-019-0169-2
pmc: PMC6727648
mid: NIHMS1048780
doi:
Substances chimiques
Inflammasomes
0
Lipoproteins
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
NLRP3 protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
389-406Subventions
Organisme : NHLBI NIH HHS
ID : R35 HL145228
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL107497
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL140554
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL132412
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL127464
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL075662
Pays : United States
Organisme : NHLBI NIH HHS
ID : K99 HL145131
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007343
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL087123
Pays : United States
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