The role of metabolic reprogramming and de novo amino acid synthesis in collagen protein production by myofibroblasts: implications for organ fibrosis and cancer.
Abstract
Fibrosis is a pathologic condition resulting from aberrant wound healing responses that lead to excessive accumulation of extracellular matrix components, distortion of organ architecture, and loss of organ function. Fibrotic disease can affect every organ system; moreover, fibrosis is an important microenvironmental component of many cancers, including pancreatic, cervical, and hepatocellular cancers. Fibrosis is also an independent risk factor for cancer. Taken together, organ fibrosis contributes to up to 45% of all deaths worldwide. There are no approved therapies that halt or reverse fibrotic disease, highlighting the great need for novel therapeutic targets. At the heart of almost all fibrotic disease is the TGF-β-mediated differentiation of fibroblasts into myofibroblasts, the primary cell type responsible for the production of collagen and other matrix proteins and distortion of tissue architecture. Recent advances, particularly in the field of lung fibrosis, have highlighted the role that metabolic reprogramming plays in the pathogenic phenotype of myofibroblasts, particularly the induction of de novo amino acid synthesis pathways that are required to support collagen matrix production by these cells. In this review, w...Continue Reading
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