IndraLab

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CYLD activates transdifferentiation. 4 / 4
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"CYLD promotes the transdifferentiation of AFs by directly binding to Nox4 through the USP structural domain, which plays a role in vascular remodeling, and CYLD can be used as a new target for vascular anti-inflammatory therapy for diseases such as abdominal aortic aneurysms [91]."
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"The silencing of CYLD significantly inhibited AF transdifferentiation and activation as evidenced by the expression of contractile proteins, the production of the proinflammatory cytokines MCP-1 (monocyte chemotactic protein 1) and IL-6 (interleukin-6), the deposition of extracellular matrix, and cell migration."
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"CYLD contributes to the transdifferentiation of AFs via deubiquitinating Nox4 and may play a role in vascular remodeling."
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"For instance, deubiquitinase CYLD stabilizes Nox 4 protein and promotes adventitial fibroblasts transdifferentiation, so as to participate in the regulation of arteriosclerosis process [ 12 ]."
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