Key result
Mitochondrial dysfunction drives macrophage polarization, emerging as a novel therapeutic target for pulmonary fibrosis.
Why the study?
Pulmonary fibrosis lacks curative treatments and its pathogenesis remains unclear, with the regulation of macrophage polarization by impaired mitochondrial function remaining largely unknown.
Highlights the role of mitochondria as key control centers for macrophage polarization in pulmonary fibrosis, suggesting novel therapeutic targets.
Answers are grounded in this paper and cite their sources.
May inform mitochondrial-targeted fibrosis research; leaves open clinical translation pending interventional trials.
Pulmonary fibrosis (PF) is a chronic, irreversible interstitial lung disease. There is no effective treatment or drug that can completely cure this disease. The pathogenesis is still unclear. In recent years, several scholars have reported that the main cause of PF is an imbalance in the inflammatory response and abnormal repair after lung injury. Lung macrophages, as immune cells in vivo, play an important role in regulating the immune response and immune tolerance and promoting lung injury repair through polarization. Recent studies have highlighted the importance of mitochondria in lung fibrosis, safeguarding cellular homeostasis and metabolic roles, and their ability to influence the progression of lung fibrosis by mediating macrophage polarization within lung cells. However, the regulation of macrophage polarization by impaired mitochondrial function remains largely unknown. In this review, we intend to summarize the associations of mitochondrial dysfunction, including mitochondrial dynamics, increased ROS production, mitochondrial DNA (mtDNA) leakage, and inflammatory vesicle activation, with the key mechanisms driving the polarization of both M1-type and M2-type macrophages, as well as further explore the role of mitochondria as key control centers for macrophage polarization, which may lead to novel therapeutic approaches to target and/or reverse disease progression.
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Zou et al. (2025) conducted a review in Pulmonary fibrosis. Mitochondrial dysfunction, including altered dynamics, ROS production, and mtDNA leakage, drives macrophage polarization and may serve as a novel therapeutic target in pulmonary fibrosis.
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