Macrophage polarization in tissue fibrosis.
Cardiac fibrosis
Kidney fibrosis
Liver fibrosis
Lung fibrosis
Macrophage polarization
Myofibroblasts
Skin fibrosis
Type 2 macrophage
Journal
PeerJ
ISSN: 2167-8359
Titre abrégé: PeerJ
Pays: United States
ID NLM: 101603425
Informations de publication
Date de publication:
2023
2023
Historique:
received:
22
02
2023
accepted:
23
08
2023
medline:
23
10
2023
pubmed:
18
10
2023
entrez:
18
10
2023
Statut:
epublish
Résumé
Fibrosis can occur in all major organs with relentless progress, ultimately leading to organ failure and potentially death. Unfortunately, current clinical treatments cannot prevent or reverse tissue fibrosis. Thus, new and effective antifibrotic therapeutics are urgently needed. In recent years, a growing body of research shows that macrophages are involved in fibrosis. Macrophages are highly heterogeneous, polarizing into different phenotypes. Some studies have found that regulating macrophage polarization can inhibit the development of inflammation and cancer. However, the exact mechanism of macrophage polarization in different tissue fibrosis has not been fully elucidated. This review will discuss the major signaling pathways relevant to macrophage-driven fibrosis and profibrotic macrophage polarization, the role of macrophage polarization in fibrosis of lung, kidney, liver, skin, and heart, potential therapeutics targets, and investigational drugs currently in development, and hopefully, provide a useful review for the future treatment of fibrosis.
Identifiants
pubmed: 37849830
doi: 10.7717/peerj.16092
pii: 16092
pmc: PMC10578305
doi:
Types de publication
Review
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e16092Informations de copyright
©2023 Yang et al.
Déclaration de conflit d'intérêts
The authors declare there are no competing interests.
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