ArticleFrontiers in molecular biosciences2025
Analysis of TGFβ1-Induced activin A gene expression in kidney mesangial cells.
Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The cytokine activin A is emerging as an important regulator of kidney fibrosis. Its expression, negligible in normal kidney, is significantly increased in various fibrotic kidney diseases. TGFβ1 is a cytokine belonging to the same family, which is well established to be a central mediator of kidney fibrosis. Although targeting TGFβ1 therapeutically is not feasible due to its homeostatic roles, we previously showed that activin A is upregulated by, and mediates the profibrotic effects of, TGFβ1. Methods: We investigated the transcriptional regulation of activin A by TGFβ1 in primary kidney mesangial cells (MC). Cells were transfected with a luciferase reporter construct containing the activin A promoter or a series of deletion constructs. Guided by MatInspector, key TGFβ1-responsive consensus elements were identified. Results: TGFβ1 increased transcription of the activin A subunit Conclusion: These findings provide insight into potential therapeutic targets for activin A targeting and attenuation of kidney fibrosis.
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