Pulmonary fibrosis is a severe disease that involves the lung parenchyma. The pattern of the disease progresses with increasing fibrosis, resulting in severe restrictive lung disease. Also, revealed that each patient normally has a median survival rate of 2 to 5 years after a diagnosis. Having said that, current treatment options focus on only alleviating the symptoms and trying to stabilise or reverse their progression, and no cure can be seen on the horizon. Some natural immunity elements play a role in the development of pulmonary fibrosis, and macrophages are among them. At first, they prevent lung injury by encouraging inflammation and attracting immune cells. However, prolonged, persistent activation has the paradoxical effect of preventing the clearance of inflammatory mediators and prolonging inflammation. This, in turn, activates the mediator-producing molecules that will lead to remodelling and fibrosis. Current investigations show that macrophages have phenotypic versatility and can enhance tissue remodelling or fibrosis, so pulmonary fibrosis may be exploited by targeting macrophages. In this review, we propose the functions of macrophages in pulmonary fibrosis: Considering polarity, activity control factors, macrophage to other cell types, and signalling networks. The issue of the potential of advertised opportunities in modulating macrophage polarisation and the developments related to the non-coding RNA drugs are also considered. Last of all, special attention should be paid to the enhancement of the investigations concerning macrophages within this disease and on experiments with different therapies for pulmonary fibrosis.
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