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OTUB2 aggravates pathological cardiac hypertrophy through Rac1 activation.

Junhui Xing1, Lijin Lin2, Yi Zhao1

  • 1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Erqi District, Zhengzhou, 450000, Henan, China.

Human Cell
|December 2, 2025
PubMed
Summary
This summary is machine-generated.

Ovarian tumor domain-containing protein 2 (OTUB2) drives pathological cardiac hypertrophy by activating Rac1 and the MEK/ERK pathway. Inhibiting this OTUB2/Rac1 axis may offer a new therapeutic target for heart remodeling.

Keywords:
Cardiac dysfunctionOTUB2Pathological cardiac hypertrophyRac1

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Pathological cardiac hypertrophy is a maladaptive response to pressure overload, progressing to heart dysfunction.
  • Understanding the molecular drivers of cardiac hypertrophy is essential for developing effective treatments.

Purpose of the Study:

  • To identify novel molecular regulators of pathological cardiac hypertrophy.
  • To elucidate the role of ovarian tumor (OTU) domain-containing ubiquitin aldehyde-binding protein 2 (OTUB2) in cardiac hypertrophy.

Main Methods:

  • Utilized transverse aortic constriction (TAC) in mice and phenylephrine (PE) stimulation in neonatal rat cardiomyocytes (NRCMs).
  • Investigated OTUB2 expression changes and functional impacts of its overexpression or knockdown.
  • Assessed cardiac remodeling, fibrosis, and cardiomyocyte size.
  • Examined the involvement of the Rac1/MEK/ERK pathway and used Rac1 inhibitor NSC23766.

Main Results:

  • OTUB2 expression was significantly upregulated in TAC-induced hypertrophy and PE-stimulated cardiomyocytes.
  • Cardiomyocyte-specific OTUB2 overexpression exacerbated TAC-induced cardiac remodeling and fibrosis.
  • OTUB2 knockdown attenuated PE-induced cardiomyocyte hypertrophy.
  • OTUB2 upregulated active Rac1, activating the MEK/ERK pathway, and Rac1 inhibition blocked OTUB2's hypertrophic effects.

Conclusions:

  • OTUB2 acts as a key regulator of pathological cardiac hypertrophy.
  • The OTUB2/Rac1/MEK/ERK signaling axis is a novel pathway implicated in cardiac remodeling.
  • Targeting the OTUB2/Rac1 axis presents a potential therapeutic strategy for cardiac hypertrophy and remodeling.