Metabolic dysregulation in pulmonary fibrosis: insights into amino acid contributions and therapeutic potential

Idiopathic pulmonary fibrosis (IPF) is a progressive and life-threatening interstitial lung disease characterized by excessive extracellular matrix deposition and fibroblast activation. Emerging evidence suggests that amino acid metabolism plays a crucial role in the pathogenesis of pulmonary fibrosis. Key amino acids, including arginine, proline, and glutamine, contribute to the regulation of fibroblast activity and collagen synthesis, all of which are essential for fibrotic progression. Studies in experimental models of pulmonary fibrosis have demonstrated significant metabolic dysregulation, further highlighting its relevance in disease development. Moreover, targeting amino acid metabolism has emerged as a promising therapeutic strategy, with novel drugs and interventions designed to modulate metabolic pathways showing potential in preclinical and clinical studies. This review explores the intricate interplay between amino acid metabolism and pulmonary fibrosis, discusses its implications for disease progression, and evaluates the therapeutic prospects of metabolic interventions in IPF management. Understanding these metabolic mechanisms may pave the way for more effective and personalized treatment strategies for IPF.