The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis

Pulmonary fibrosis is a chronic debilitating condition characterized by progressive deposition of connective tissue, leading to a steady restriction of lung elasticity, a decline in lung function, and a median survival of 4.5 years. The leading causes of pulmonary fibrosis are inhalation of foreign particles (such as silicosis and pneumoconiosis), infections (such as post COVID-19), autoimmune diseases (such as systemic autoimmune diseases of the connective tissue), and idiopathic pulmonary fibrosis. The therapeutics currently available for pulmonary fibrosis only modestly slow the progression of the disease. This review is centered on the interplay of damage-associated molecular pattern (DAMP) molecules, Toll-like receptor 4 (TLR4), and inflammatory cytokines (such as TNF-alpha, IL-1 beta, and IL-17) as they contribute to the pathogenesis of pulmonary fibrosis, and the possible avenues to develop effective therapeutics that disrupt this interplay.

Automated summary

Pulmonary fibrosis is a chronic condition characterized by progressive deposition of connective tissue, leading to a decline in lung elasticity and function. Common causes include inhalation of foreign particles, infections, autoimmune diseases, and idiopathic pulmonary fibrosis. Current therapeutics only modestly slow disease progression. This review focuses on the interplay of DAMP molecules, TLR4, and inflammatory cytokines in the pathogenesis of pulmonary fibrosis and explores potential avenues for developing effective therapeutics.