Effect and significance of TGF-β1 in the process of radiation fibrosis
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Radiation fibrosis of human normal tissues is very common in radiotherapy. One of the main fundamental problems yet unsolved in fibrotic tissues is the origin of the chronic activation of myofibroblasts within these tissues. It has been postulated by some researchers that this chronic activation results from a continuous production of activating factors. So fibrosis could be defined as a wound where continuous signals for repair are emitted. Cytokines and growth factors probably play a vital role in this process. Among them transforming growth factor β1(TGF β1) is considered as a master switch for the fibrotic program. This review discusses recent evidence on the critical role played by TGF β1 in the initiation, development, and persistence of radiation fibrosis. It summarized the results concerning this factor after irradiation of various tissues and cells. All these researches show that the TGF β1 pathway may be a specific target for anti fibrotic agents. [Keywords:
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Fibrotic disease is a type of disease in which the body is affected by various stimulating factors, which causes the activation or phenotypic transformation of myofibroblasts, increases the expression of collagen and excessive deposition of extracellular matrix, resulting in damage to the structure and function of organs. Transforming growth factor-β (TGF-β) is currently recognized as a signal transduction pathway involved in the occurrence of fibrotic diseases, and plays an important role in regulating the occurrence and development of fibrotic diseases such as lung, liver, myocardium, kidney and pancreas. In recent years, many studies have explored the role of TGF-β signaling pathway in the occurrence and development of fibrotic diseases, while to inhibit the activation of TGF-β signaling pathway might have anti-fibrosis effects, but the mechanism has not been fully understood. Therefore, the research progress of the role of TGF-β signaling pathway in such fibrotic diseases as lung, liver, myocardium, kidney and pancreas, and so on, has mainly been reviewed in present paper, so as to provide new strategies for the selection of therapeutic targets for fibrotic diseases.
DOI: 10.11855/j.issn.0577-7402.2020.11.11
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The number of cancer survivors in the US is increasing exponentially and currently approaches 10 million. While long-term cancer survivors may be cured of their original malignancies, some suffer from treatment-related side effects. Radiation injury of normal tissues, particularly radiation-induced fibrosis, is a major contributor to long-term morbidity after cancer therapy. Among the fibrogenic factors that have been investigated in the context of radiation fibrosis, transforming growth factor-β (TGF-β) appears to play a particularly central role. Consequently, considerable efforts have been directed toward targeting TGF-β or TGF-∇ signaling as a strategy to prevent or treat radiation fibrosis. This chapter discusses the clinical significance of long-term side effects after cancer therapy with special emphasis on intestinal radiation fibrosis. Existing evidence in support of a mechanistic role for TGF-β is introduced and discussed, and various approaches by which chronic radiation fibrosis may be ameliorated by inhibition of the TGF-β signaling pathway are presented.
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Lung Fibrosis
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Transforming growth factor-β(TGF-β) is the adjusted factor, involving in progress of pulmonary inflammation, and also involving in chronic tissue reparation. TGF-β is a member of cytokine family involving in pulmonary fibrosis effected by TGF-β. The isoform's activities of TGF-β are closely related to its types and receptors' affinity. The signal pathways of TGF-β are believed to be primarily responsible for pulmonary fibrosis progression.
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Pulmonary fibrosis; Transforming growth factor-β1; Transforming growth factor-β1; Signalpathway
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In human tissues, normal homeostasis requires intricately balanced interactions between cells and the network of secreted proteins known as the extracellular matrix. These cooperative interactions involve numerous cytokines acting through specific cell-surface receptors. When the balance between the cells and the extracellular matrix is perturbed, disease can result. This is clearly evident in the interactions mediated by the cytokine transforming growth factor-(TGF-. TGF-signaling has been studied extensively in fibrotic disease of lung, liver, skin, and kidney. However, little is known about the role of TGF-in bladder fibrosis. This review focuses on the mechanisms underlying TGF beta expression and how it relates to fibrotic processes in bladder.
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Renal fibrosis is the final common pathway of several nephropathies including chronic allograft failure. Most chronic renal diseases result in tissue fibrosis, and this is independent of their initial cause. Tissue fibrosis is an accumula- tion of extracellular matrix, and in animal models of renal fibrosis, mRNA levels for profibrogenic cytokines such as transforming growth factor � (TGF�) and extracellular matrix (ECM) molecular components are up regulated and they precede glomerulosclerosis and interstitial fibrosis. TGF� 1 plays a crucial role in renal fibrosis. In this review the main features of this important cytokine and existing previous therapeutic attempts to inhibit TGFexpression are briefly sum- marised.
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Fibrosis involves an orchestrated cascade of events including activation of fibroblasts, increased production and deposition of extracellular matrix components, and differentiation of fibroblasts into myofibroblasts. Epithelial-mesenchymal cross-talk plays an important role in this process, and current hypotheses of organ fibrosis liken it to an aberrant wound healing response in which epithelial-mesenchymal transition (EMT) and cellular senescence may also contribute to disease pathogenesis. The fibrotic response is associated with altered expression of growth factors and cytokines, including increased levels of transforming growth factor-β1 (TGF-β1) and the more recent observation that increased levels of several insulin-like growth factor binding proteins (IGFBPs) are associated with a number of fibrotic conditions. IGFBPs have been implicated in virtually every cell type and process associated with the fibrotic response, making the IGFBPs attractive targets for the development of novel anti-fibrotic therapies. In this review, the current state of knowledge regarding the classical IGFBP family in organ fibrosis will be summarized and the clinical implications considered.
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