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Updated: Aug 12, 2025

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Hyperactivation of YAP/TAZ Drives Alterations in Mesangial Cells through Stabilization of N-Myc in Diabetic

Seunghyeok Choi1, Seon Pyo Hong2, Jung Hyun Bae2

  • 1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.

Journal of the American Society of Nephrology : JASN
|February 1, 2023
PubMed
Abstract

Insights

High glucose activates YAP/TAZ in kidney mesangial cells, leading to N-Myc stabilization and diabetic nephropathy (DN). Lowering blood glucose may delay DN progression.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Diabetology

Background:

  • Kidney mesangial cells (MCs) are crucial for glomerular integrity.
  • MC dysfunction underlies diabetic nephropathy (DN).
  • High blood glucose impairs MCs, but mechanisms are unclear.

Purpose of the Study:

  • Investigate the role of YAP/TAZ in high glucose-induced MC alterations.
  • Elucidate the molecular mechanisms linking high glucose to DN pathogenesis.
  • Identify potential therapeutic targets for DN.

Main Methods:

  • Analyzed YAP/TAZ and MC pathology in human DN patients and animal models.
  • Used RiboTag sequencing to profile MC gene expression.
  • Performed immunoprecipitation to assess protein interactions and stability.

Main Results:

  • YAP/TAZ are elevated in MCs from DN patients and models.
  • High glucose directly activates YAP/TAZ via the Hippo pathway in cultured MCs.
  • YAP/TAZ hyperactivation in mice mimics DN hallmarks, stabilizing N-Myc and enhancing its activity.

Conclusions:

  • High glucose activates YAP/TAZ, leading to N-Myc stabilization and MC dysfunction in DN.
  • This pathway provides insight into DN pathogenesis.
  • Blood glucose control may mitigate DN progression.

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