Proceedings of the American Thoracic Society
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Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that healthcare recommendations are informed by the best available research evidence. This is the fourth of a series of 14 articles prepared to advise guideline developers in respiratory and other disease. It focuses on commercial funding of guidelines and managing conflict of interest effectively in the context of guidelines. ⋯ Professional societies often depend on industry funding to support clinical practice guideline development. In addition, members of guideline committees frequently have financial relationships with commercial entities, are invested in their intellectual work, or have conflicts related to clinical revenue streams. No systematic reviews or other rigorous evidence regarding best practices for funding models, disclosure mechanisms, management strategies, or enforcement presently exist, but the panel drew several conclusions that could improve transparency and process.
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Transforming growth factor-β (TGF-β) is extensively involved in the development of fibrosis in different organs. Overproduction or potentiation of its profibrotic effects leads to an aberrant wound healing response during the initiation of fibrotic processes. ⋯ In addition, excess extracellular matrix production contributes in a major way to disease pathogenesis. For this reason, this review will focus on discussing novel data and highlight growing interest in deepening the understanding of the profibrotic role of TGF-β and its direct or indirect targeting for disease modulation.
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Although substantial progress has been made in understanding the clinical, radiological, and pathological manifestations of fibrosing interstitial lung diseases (ILD), it remains difficult for the clinician to predict the clinical course or the response to therapy for the subtypes of ILD, even from individual to individual with the same diagnosis. This article reviews the genetic and environmental causes of pulmonary fibrosis, specifically focusing on genetic and epigenetic variants of MUC5B and several types of ILD, to discuss why only some individuals with the MUC5B promoter polymorphism develop pulmonary fibrosis. Once we discover how these genetic and epigenetic risks lead to the development of ILD, we and others can apply these discoveries to: (1) identify individuals at risk of developing ILD, (2) diagnose the condition at an earlier stage, (3) identify novel mechanisms that cause ILD, and (4) eventually develop personalized therapeutic strategies for intervention.