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PON2 ameliorates Ang II-induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway

Yuanzheng Ye1,2, Jian Zhang3, Yankai Guo2,4

  • 1Department of Cardiac Function, State Key Laboratory of Pathogenesis Prevention and Treatment of High Incidence Diseases in Central Asia, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.

Immunity, Inflammation and Disease
|February 25, 2023
PubMed
Abstract

Insights

Paraoxonase 2 (PON2) protects against heart failure by inhibiting oxidative stress, inflammation, and cardiomyocyte damage. This study reveals PON2 targets CANX/NOX4 signaling to ease injury in heart failure models.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Heart failure (HF) incidence is rising globally, second only to cancer.
  • Limited research exists on paraoxonase 2 (PON2) roles in HF, despite its known cardiovascular protective effects.

Purpose of the Study:

  • To investigate the role of paraoxonase 2 (PON2) in angiotensin II (Ang II)-induced heart failure.
  • To elucidate the underlying molecular mechanisms involving PON2 in cardiomyocyte injury.

Main Methods:

  • Assessed PON2 expression in Ang II-challenged AC16 cells using RT-qPCR and Western blot.
  • Quantified reactive oxygen species, oxidative stress, inflammation, and apoptosis.
  • Analyzed cytoskeleton and hypertrophy-related proteins, and investigated PON2-Calnexin (CANX) interactions via database analysis and co-immunoprecipitation.

Main Results:

  • PON2 expression was reduced in Ang II-induced AC16 cells.
  • PON2 mediated the inhibition of oxidation, inflammation, hypertrophy, and damage.
  • PON2 appears to act via the CANX/NOX4 signaling pathway.

Conclusions:

  • Paraoxonase 2 (PON2) alleviates Ang II-induced cardiomyocyte injury.
  • The protective effect of PON2 is achieved by targeting the CANX/NOX4 signaling pathway.
Keywords:
Ang II-induced cardiomyocyte injuryCANX/NOX4 signaling pathwayPON2heart failure

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