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Shared mechanisms of organ fibrosis
Benjamin D. Humphreys
Benjamin D. Humphreys
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Review

Shared mechanisms of organ fibrosis

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Abstract

Organ fibrosis involves a complex interplay between diverse cell types and signaling pathways that ultimately leads to the pathologic accumulation of excessive extracellular matrix, subsequently resulting in organ dysfunction. In recent years, the first drugs for the treatment of idiopathic pulmonary fibrosis have been approved; however, there is a major unmet need for effective antifibrotic therapies across organs. Despite the complexity of the fibrotic process in different tissues, certain features are shared and may form the basis for future therapeutic strategies. This Review will highlight these shared characteristics, cell states, and signaling pathways across organs with the goal of highlighting potential antifibrotic strategies.

Authors

Benjamin D. Humphreys

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Figure 2

Mechanosensation and fibrosis.

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Mechanosensation and fibrosis.
Cells detect stiffness primarily through ...
Cells detect stiffness primarily through integrin receptors that bind ECM. This activates FAK, which phosphorylates SRC, relieving inhibition of the Hippo pathway. This causes YAP dephosphorylation, translation into the nucleus, and transcription of profibrogenic genes. Stiffness within the cell is also detected by mechanical pathways, which can independently activate YAP. TEAD, TEA domain transcription factor.

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ISSN 2379-3708

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