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SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism

Aihua Yang1, Jiaxin Cao1, Jiaona Gu1

  • 1Department of Pharmacology, School of Medicine and School of Pharmacy, Nantong University, Nantong, 226001, China.

Scientific Reports
|July 2, 2025
PubMed

Insights

SH3 domain binding kinase family member 3 (SBK3) is a novel mitochondrial protein that suppresses pathological cardiac hypertrophy. Maintaining SBK3 levels protects against heart failure by rebalancing oxidative stress and energy metabolism.

Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Molecular Medicine

Background:

  • Pathological cardiac hypertrophy is a risk factor for heart failure, associated with elevated renin-angiotensin II (Ang II) and catecholamines.
  • SH3 domain binding kinase family member 3 (SBK3) is a mitochondrial protein highly expressed in cardiac tissue.

Purpose of the Study:

  • To investigate the role of SBK3 in Ang II-induced cardiac hypertrophy.
  • To explore SBK3 as a potential therapeutic target for cardiac hypertrophy and heart failure by modulating mitochondrial function.

Main Methods:

  • Determined mitochondrial localization of SBK3 in rat cardiomyocytes.
  • Assessed SBK3 protein expression in Ang II-perfused mouse hearts.
  • Evaluated the effects of SBK3 overexpression on Ang II-induced cardiac hypertrophy in vitro and in vivo.
  • Analyzed oxidative stress, energy metabolism, and dynamin-related protein 1 (Drp1) phosphorylation at serine 616 (S616).

Main Results:

  • SBK3 was localized to mitochondria in rat cardiomyocytes.
  • SBK3 protein expression decreased in Ang II-perfused mouse hearts.
  • Maintaining high SBK3 levels significantly suppressed Ang II-induced cardiac hypertrophy.
  • SBK3 overexpression rebalanced Ang II-induced oxidative stress and energy metabolism, inhibiting Drp1 S616 phosphorylation.

Conclusions:

  • SBK3 is a novel mitochondrial protein that suppresses cardiac hypertrophy.
  • SBK3 plays a protective role against Ang II-induced cardiac hypertrophy by regulating mitochondrial function and cellular stress pathways.

Keywords:
Drp1HeartHypertrophyMitochondriaSBK3

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