Profibrotic macrophage populations and cell communications in pulmonary fibrosis

• Autores: Dongfeng Zhang, Wenyue Zhao, Chang Xu, Liping Bu, Qiang Liu
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 82, Nº. 1, 2026
• Idioma: inglés
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• Resumen

  • Pulmonary fibrosis is a chronic inflammatory disorder marked by fibroblast activation, collagen deposition, thickening of the alveolar septum, and impaired lung function. Profibrotic macrophages play a pivotal role in driving inflammatory responses during the progression of pulmonary fibrosis and have emerged as promising therapeutic targets. Although distinct from classical M1/M2 macrophage phenotypes, profibrotic macrophages across various forms of pulmonary fibrosis exhibit shared transcriptomic profiles associated with fibrogenesis. This review aims to summarize the characteristics, origins, developmental trajectories, distribution, energy metabolism, and epigenetic regulation of profibrotic macrophage populations in different pulmonary fibrosis diseases and animal models. In the context of pulmonary fibrosis, these macrophages engage in robust crosstalk with non-immune cells in the lung—such as fibroblasts and type II alveolar epithelial cells—thereby exacerbating fibrotic processes. Consequently, strategies aimed at depleting profibrotic macrophages or disrupting their detrimental interactions with non-immune cells may show promise as potential therapeutic approaches to slow disease progression, offering new avenues for treatment.