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TEA domain transcription factor 3 suppresses aortic and left ventricular remodeling via transcriptional activation of

Lei Wang1, Yufeng Bai2, Dan Ma2

  • 1Department of Medical Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China.

Biochemical Pharmacology
|September 12, 2025
PubMed

Insights

Hypertension causes cardiovascular remodeling. This study found that increasing TEA domain transcription factor 3 (TEAD3) expression protects blood vessels by upregulating PDZ domain-containing 1 (PDZK1), reducing cell growth and migration, and improving heart structure.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Hypertension Research

Background:

  • Hypertension induces pathological vascular and ventricular remodeling, increasing cardiovascular disease risk.
  • TEA domain transcription factor 3 (TEAD3) is highly expressed in the heart, and PDZ domain-containing 1 (PDZK1) protects blood vessels.
  • Reduced TEAD3 and PDZK1 expression was observed in the aortas of spontaneously hypertensive rats (SHRs).

Purpose of the Study:

  • To investigate the role of TEAD3 in hypertension-induced cardiovascular remodeling.
  • To elucidate the molecular mechanisms by which TEAD3 exerts its protective effects.
  • To explore the therapeutic potential of targeting the TEAD3-PDZK1 axis.

Main Methods:

  • Adeno-associated virus delivery was used to overexpress TEAD3 in SHR vascular smooth muscle cells (VSMCs).
  • Adenoviral infection was employed to overexpress TEAD3 or PDZK1 in SHR-derived VSMCs.
  • DNA pull-down assays and PDZK1 knockdown were utilized to confirm TEAD3-PDZK1 interaction and function.

Main Results:

  • TEAD3 overexpression alleviated aortic remodeling by reducing elastic fiber and collagen deposition, thereby attenuating hypertension.
  • TEAD3 overexpression and PDZK1 overexpression/upregulation suppressed VSMC proliferation and migration.
  • TEAD3 directly binds to the PDZK1 promoter, upregulating PDZK1 expression, which inhibits the PI3K/Akt pathway via phosphoinositide-3-kinase adaptor protein 1.

Conclusions:

  • The TEAD3-PDZK1 axis mitigates abnormal VSMC proliferation and migration.
  • This axis ameliorates aortic and left ventricular remodeling in hypertensive conditions.
  • The findings provide a molecular basis for developing targeted therapies against hypertension-induced cardiovascular remodeling.

Keywords:
HypertensionPDZ domain containing 1TEA domain transcription factor 3Vascular smooth muscle cellVentricular and vascular remodeling

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