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My research focuses on identifying the mechanisms leading to lung fibrosis, or scarring. In the lung, idiopathic pulmonary fibrosis (IPF) is a disease characterized by progressive fibrosis of unclear etiology, resulting in the rapid development of respiratory failure and death. Myofibroblasts are the key effector cells in fibrotic diseases and are responsible for producing excessive extracellular matrix proteins. We have recently reported that the mechanistic target of rapamycin (mTOR) reconfigures the myofibroblast metabolic network to meet the biosynthetic demands associated with enhanced matrix biosynthesis. This new field, coined fibrometabolism, has emerged as an important research topic, given that it may offer a novel approach to target IPF and other fibrotic diseases.
Selvarajah B, Azuelos I, Platé M, Guillotin D, Forty EJ, Contento G, Woodcock HV, Redding M, Taylor A, Brunori G, Durrenberger PF, Ronzoni R, Blanchard AD, Mercer PF, Anastasiou D, Chambers RC. mTORC1 amplifies the ATF4-dependent de novo serine-glycine pathway to supply glycine during TGF-β1-induced collagen biosynthesis. Sci Signal. 2019;12(582): eaav3048. Published 2019 May 21. doi:10.1126/scisignal.aav3048. PMID: 31113850.