The Role of Macrophages in Lung Fibrosis and the Signaling Pathway

© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature..

Lung fibrosis is a dysregulated repair process caused by excessive deposition of extracellular matrix that can severely affect respiratory function. Macrophages are a group of immune cells that have multiple functions and can perform a variety of roles. Lung fibrosis develops with the involvement of pro-inflammatory and pro-fibrotic factors secreted by macrophages. The balance between M1 and M2 macrophages has been proposed to play a role in determining the trend and severity of lung fibrosis. New avenues and concepts for preventing and treating lung fibrosis have emerged in recent years through research on mitochondria, Gab proteins, and exosomes. The main topic of this essay is the impact that mitochondria, Gab proteins, and exosomes have on macrophage polarization. In addition, the potential of these factors as targets to enhance lung fibrosis is also explored. We have also collated the functions and mechanisms of signaling pathways associated with the regulation of macrophage polarization such as Notch, TGF-β/Smad, JAK-STAT and cGAS-STING. The goal of this article is to explain the potential benefits of focusing on macrophage polarization as a way to relieve lung fibrosis. We aspire to provide valuable insights that could lead to enhancements in the treatment of this condition.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - year:2024

Enthalten in:

Cell biochemistry and biophysics - (2024) vom: 27. März

Sprache:

Englisch

Beteiligte Personen:

Wang, Xingmei [VerfasserIn]
Zhou, Jiaxu [VerfasserIn]
Li, Xinrui [VerfasserIn]
Liu, Chang [VerfasserIn]
Liu, Lan [VerfasserIn]
Cui, Hong [VerfasserIn]

Links:

Volltext

Themen:

Journal Article
M1-type macrophages
M2-type macrophages
Macrophage polarization
Macrophages
Pulmonary fibrosis
Review

Anmerkungen:

Date Revised 27.03.2024

published: Print-Electronic

Citation Status Publisher

doi:

10.1007/s12013-024-01253-5

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM370261305