Journal
SCIENCE SIGNALING
Volume 14, Issue 697, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aay1027
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Funding
- MRC [MC_UP_1202/1] Funding Source: UKRI
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Fibrosis is the final pathological outcome and main cause of morbidity and mortality in many common and chronic diseases, with an increased interest in the application of omics technologies to identify new therapeutic targets and disease biomarkers. Metabolic alterations, particularly in myofibroblasts, may play a significant role in the pathogenesis of fibrosis, especially in diseases like idiopathic pulmonary fibrosis.
Fibrosis is the final pathological outcome and major cause of morbidity and mortality in many common and chronic inflammatory, immune-mediated, and metabolic diseases. Despite the growing incidence of fibrotic diseases and extensive research efforts, there remains a lack of effective therapies that improve survival. The application of omics technologies has revolutionized our approach to identifying previously unknown therapeutic targets and potential disease biomarkers. The application of metabolomics, in particular, has improved our understanding of disease pathomechanisms and garnered a wave of scientific interest in the role of metabolism in the biology of myofibroblasts, the key effector cells of the fibrogenic response. Emerging evidence suggests that alterations in metabolism not only are a feature of but also may play an influential role in the pathogenesis of fibrosis, most notably in idiopathic pulmonary fibrosis (IPF), the most rapidly progressive and fatal of all fibrotic conditions. This review will detail the role of key metabolic pathways, their alterations in myofibroblasts, and the potential this new knowledge offers for the development of antifibrotic therapeutic strategies.
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