Macrophage polarization and its impact on idiopathic pulmonary fibrosis

Macrophage polarization and its impact on idiopathic pulmonary fibrosis

26 July 2024 | Zhouling Ge, Yong Chen, Leikai Ma, Fangjun Hu and Lubin Xie
This review article by Zhouling Ge, Yong Chen, Leikai Ma, Fangjun Hu, and Lubin Xie explores the role of macrophage polarization in idiopathic pulmonary fibrosis (IPF). IPF is a progressive lung disease characterized by chronic pulmonary fibrosis, leading to respiratory failure and death. The incidence and prevalence of IPF are increasing globally, and current treatments are limited to lung transplantation, which is only suitable for a minority of patients. The authors highlight the importance of macrophages in IPF, as they play a crucial role in immune function, tissue remodeling, and inflammatory response. Macrophages can be divided into two main phenotypes: M1 (inflammatory) and M2 (anti-inflammatory). M1 macrophages are associated with pro-inflammatory effects and can promote fibroblast proliferation and extracellular matrix (ECM) deposition, while M2 macrophages exhibit anti-inflammatory and tissue repair functions. The balance between M1 and M2 macrophages is critical for disease progression. The article discusses the metabolic reprogramming of macrophages, including glucose, amino acid, and fatty acid metabolism, which influence their polarization. Mitochondrial function, endoplasmic reticulum (ER) stress, mechanotransduction, and epigenetic regulation are also explored as key factors in macrophage polarization. The authors emphasize the complex interplay between these factors and their impact on IPF pathogenesis. Understanding the mechanisms of macrophage polarization is essential for developing more effective therapeutics for IPF.This review article by Zhouling Ge, Yong Chen, Leikai Ma, Fangjun Hu, and Lubin Xie explores the role of macrophage polarization in idiopathic pulmonary fibrosis (IPF). IPF is a progressive lung disease characterized by chronic pulmonary fibrosis, leading to respiratory failure and death. The incidence and prevalence of IPF are increasing globally, and current treatments are limited to lung transplantation, which is only suitable for a minority of patients. The authors highlight the importance of macrophages in IPF, as they play a crucial role in immune function, tissue remodeling, and inflammatory response. Macrophages can be divided into two main phenotypes: M1 (inflammatory) and M2 (anti-inflammatory). M1 macrophages are associated with pro-inflammatory effects and can promote fibroblast proliferation and extracellular matrix (ECM) deposition, while M2 macrophages exhibit anti-inflammatory and tissue repair functions. The balance between M1 and M2 macrophages is critical for disease progression. The article discusses the metabolic reprogramming of macrophages, including glucose, amino acid, and fatty acid metabolism, which influence their polarization. Mitochondrial function, endoplasmic reticulum (ER) stress, mechanotransduction, and epigenetic regulation are also explored as key factors in macrophage polarization. The authors emphasize the complex interplay between these factors and their impact on IPF pathogenesis. Understanding the mechanisms of macrophage polarization is essential for developing more effective therapeutics for IPF.
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