Chemokines in cardiac fibrosis.
chemokine
extracellular matrix
fibroblast
fibrosis
heart failure
macrophage
myocardial infarction
Journal
Current opinion in physiology
ISSN: 2468-8673
Titre abrégé: Curr Opin Physiol
Pays: England
ID NLM: 101715200
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
entrez:
16
11
2020
pubmed:
17
11
2020
medline:
17
11
2020
Statut:
ppublish
Résumé
Several members of the chemokine family are involved in regulation of fibrosis. This review manuscript discusses the role of the chemokines in the pathogenesis of myocardial fibrosis. The CC chemokine CCL2 exerts fibrogenic actions through recruitment and activation of monocytes and macrophages expressing its receptor, CCR2. Other CC chemokines may also contribute to fibrotic remodeling by recruiting subsets of fibrogenic macrophages. CXC chemokines containing the ELR motif may exert pro-fibrotic actions, through recruitment of activated neutrophils and subsequent formation of neutrophil extracellular traps (NETs), or via activation of fibrogenic monocytes. CXCL12 has also been suggested to exert fibrogenic actions through effects on fibroblasts and immune cells. In contrast, the CXCR3 ligand CXCL10 was found to reduce cardiac fibrosis, inhibiting fibroblast migration. Chemokines are critical links between inflammation and fibrosis in myocardial disease and may be promising therapeutic targets for patients with heart failure accompanied by prominent inflammation and fibrosis.
Identifiants
pubmed: 33195890
doi: 10.1016/j.cophys.2020.10.004
pmc: PMC7665080
mid: NIHMS1638956
doi:
Types de publication
Journal Article
Langues
eng
Pagination
80-91Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL076246
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL085440
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL149407
Pays : United States
Déclaration de conflit d'intérêts
CONFLICT OF INTEREST STATEMENT: The authors have no conflicts to disclose.
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