Advances in metabolic reprogramming of pulmonary fibrosis

Abstract

Pulmonary fibrosis (PF) refers to a common pathological change that occurs in a series of lung diseases. It is manifested by fibroblast proliferation and excessive extracellular matrix (ECM) deposition, resulting in destruction of lung structure and deterioration of lung function. PF represents a widespread global health problem, particularly in developing countries, and poses a substantial threat to public health. Despite its clinical significance, effective and specific pharmacological therapies remain unavailable. Therefore, identifying novel therapeutic targets is urgently needed and holds considerable clinical importance. A clearer understanding of the underlying pathogenic mechanisms of PF is essential for improving both prevention and treatment strategies. In recent years, increasing evidence has indicated that metabolic reprogramming including alterations in glucose, lipid, and amino acid metabolism plays an important role in the initiation and progression of PF. In this review, we summarize current knowledge regarding metabolic reprogramming in PF and highlight the potential of metabolic pathways as targets for diagnosis and therapy, thereby offering new perspectives for future research.