We will notify you of the publication of new articles in BIO integration. Pulmonary fibrosis (PF) is a progressive and irreversible interstitial lung disease characterized by destruction of alveolar structures, excessive proliferation of fibroblasts, and abnormal deposition of extracellular matrix (ECM), but the exact pathogenesis is still not completely understood.
Although lactate has traditionally been regarded as the final metabolite of glycolysis, it is being reevaluated as an important signaling molecule that can actively modulate a variety of cellular functions, especially with the rise of the concept of metabolic reprogramming after the Warburg effect. Among these cellular functions, lactate-induced post-translational modification (PTM) known as lactylation provides a new perspective for understanding the wide range of biological actions of lactate beyond metabolism.
Of note, the pathological microenvironment of PF is characterized by extensive metabolic reprogramming and lactate accumulation, suggesting that lactate and lactate-mediated lactylation may play an important role in disease progression by modulating the expression of profibrotic genes and influencing fibroblast activation and differentiation.
This review paper focuses on how lactylation acts as a bridge connecting metabolic reprogramming and fibrotic phenotype in PF and discusses its potential translation as a novel therapeutic target.
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Reference magazines:
Wang, F. Others. (2026) Lactate and lactylation in the progression of pulmonary fibrosis. BIO integration. DOI: 10.15212/bioi-2026-0009. https://www.scienceopen.com/hosted-document?doi=10.15212/bioi-2026-0009
