Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis
Amit Kishore1,2, Martin Petrek1,3,4
1Department of Pathological Physiology, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czechia.
Abstract:
This mini-review summarizes the current evidence for the role of macrophage activation and polarization in inflammation and immune response pertinent to interstitial lung disease, specifically pulmonary fibrosis. In the fibrosing lung, the production and function of inflammatory and fibrogenic mediators involved in the disease development have been reported to be regulated by the effects of polarized M1/M2 macrophage populations. The M1 and M2 macrophage phenotypes were suggested to correspond with the pro-inflammatory and pro-fibrogenic signatures, respectively. These responses towards tissue injury followed by the development and progression of lung fibrosis are further regulated by macrophage-derived microRNAs (miRNAs). Besides cellular miRNAs, extracellular exosomal-miRNAs derived from M2 macrophages have also been proposed to promote the progression of pulmonary fibrosis. In a future perspective, harnessing the noncoding miRNAs with a key role in the macrophage polarization is, therefore, suggested as a promising therapeutic strategy for this debilitating disease.
Insights
Macrophage polarization (M1/M2) influences inflammation and fibrosis in interstitial lung disease. Targeting macrophage-derived microRNAs (miRNAs) offers a promising therapeutic strategy for pulmonary fibrosis.
Area of Science:
- Immunology
- Pulmonary Medicine
- Cell Biology
Background:
- Interstitial lung disease (ILD), particularly pulmonary fibrosis, involves complex inflammatory and immune responses.
- Macrophage activation and polarization are critical regulators of these responses in the fibrosing lung.
- Specific macrophage phenotypes, M1 (pro-inflammatory) and M2 (pro-fibrogenic), play distinct roles in disease pathogenesis.
Purpose of the Study:
- To review the current evidence on macrophage polarization in interstitial lung disease.
- To elucidate the role of M1 and M2 macrophages in regulating inflammatory and fibrogenic mediators.
- To explore the involvement of macrophage-derived microRNAs (miRNAs) in the progression of pulmonary fibrosis.
Main Methods:
- Literature review of studies investigating macrophage polarization in pulmonary fibrosis.
- Analysis of research on M1/M2 macrophage phenotypes and their associated mediators.
- Examination of the role of cellular and exosomal microRNAs in macrophage-driven fibrosis.
Main Results:
- Polarized M1/M2 macrophage populations regulate inflammatory and fibrogenic mediators in pulmonary fibrosis.
- M1 macrophages are associated with pro-inflammatory signatures, while M2 macrophages exhibit pro-fibrogenic signatures.
- Macrophage-derived microRNAs (miRNAs), including exosomal miRNAs from M2 macrophages, contribute to the development and progression of lung fibrosis.
Conclusions:
- Macrophage polarization is a key factor in the pathogenesis of pulmonary fibrosis.
- Macrophage-derived miRNAs are significant regulators of fibrotic processes.
- Targeting microRNAs involved in macrophage polarization presents a potential therapeutic avenue for pulmonary fibrosis.
