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September 1, 2024

not-yet-known not-yet-known not-yet-known unknown Diminished nuclear-localized β-adrenergic signaling activates YAP to promote kidney fibrosis in diabetic nephropathy

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Authors

WXWenjing XiangLLLei LiMQManman Qin

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Overview

Preclinical study demonstrates that diminished nuclear beta-adrenergic signaling triggers YAP-driven fibrosis in diabetic mice, suggesting PDE4 inhibition as a therapeutic strategy.

Key Points

  • Diminished nuclear cAMP signaling activates the YAP pathway to promote kidney fibrosis, while rolipram treatment restores kidney filtration function.
  • Analysis of db/db mice and cultured mesangial cells using subcellular FRET biosensors tracked adrenergic signaling microdomains following TGF-β exposure.
  • Targeting PDE4 to restore nuclear adrenergic signaling highlights a promising therapeutic strategy against diabetic nephropathy; mouse model warrants translation.

Cite This Study

Xiang et al. (2024) studied this question.

synapsesocial.com/papers/68e59e8eb6db643587538746https://doi.org/10.22541/au.172518446.62912572/v1
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Diminished nuclear‐localized <i>β</i>‐adrenoceptor signalling activates YAP to promote kidney fibrosis in diabetic nephropathy2024 · 6 citations
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  4. 4Uncovering key markers and therapeutic targets for renal fibrosis in diabetic kidney disease through bulk and single-cell RNA sequencing2025 · 11 citations
  5. 5Yes-Associated Protein is Involved in Myocardial Fibrosis in Rats with Diabetic Cardiomyopathy2021 · 10 citations