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      Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases.

      The Journal of clinical investigation

      Angiotensin II, physiology, Cell Proliferation, Chronic Disease, Embryonic Stem Cells, transplantation, Fibroblasts, pathology, Fibrosis, etiology, immunology, therapy, Humans, Infection, Neovascularization, Pathologic, metabolism, Transforming Growth Factor beta1, Wound Healing

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          Abstract

          Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.

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          Journal
          17332879
          1804380
          10.1172/JCI31487

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