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Matrix protein Tenascin-C promotes kidney fibrosis via STAT3 activation in response to tubular injury - Cell Death & Disease

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Matrix protein Tenascin-C promotes kidney fibrosis via STAT3 activation in response to tubular injury - Cell Death & Disease

Accumulating evidence indicates that the extracellular matrix (ECM) is not only a consequence of fibrosis, but also contributes to the progression of fibrosis, by creating a profibrotic microenvironment. Tenascin-C (TNC) is an ECM glycoprotein that contains multiple functional domains. We showed that following kidney injury, TNC was markedly induced in fibrotic areas in the kidney from both mouse models and humans with kidney diseases.

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Matrix protein Tenascin-C promotes kidney fibrosis via STAT3 activation in response to tubular injury - Cell Death & Disease

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Matrix protein Tenascin-C promotes kidney fibrosis via STAT3 activation in response to tubular injury - Cell Death & Disease

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