Effect of Secreted Frizzled-Related Protein 5 in Mice with Heart Failure

Pan Hong1, Lijie Wang1, Hongchao Wang1

  • 1Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang 050017, China.

Insights

Secreted frizzled-related protein 5 (SFRP5) demonstrates a protective effect against isoproterenol-induced heart failure in mice. SFRP5 may serve as a therapeutic target by inhibiting the Wnt5A/JNK pathway, reducing oxidative stress and inflammation.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Heart failure remains a significant global health concern despite treatment advancements.
  • Understanding novel therapeutic targets is crucial for improving patient outcomes.
  • Secreted frizzled-related protein 5 (SFRP5) role in cardiac function requires further elucidation.

Purpose of the Study:

  • To investigate the cardioprotective effects of SFRP5 in a mouse model of heart failure.
  • To explore the underlying molecular mechanisms of SFRP5 action in cardiac dysfunction.

Main Methods:

  • A mouse model of heart failure was induced using isoproterenol (ISO) hydrochloride.
  • Mice received intraperitoneal injections of SFRP5 recombinant protein or phosphate-buffered saline (PBS).
  • Cardiac function, myocardial histology, protein expression (SFRP5, Wnt5a, JNK), and serum enzyme activities (SOD, GSH-Px) were assessed.

Main Results:

  • SFRP5 administration reduced inflammation and improved left ventricular systolic and diastolic function.
  • SFRP5 treatment enhanced myocardial tissue structure in heart failure mice.
  • SFRP5 increased its own protein levels while decreasing Wnt5a and JNK expression, alongside elevated SOD and GSH-Px activities.

Conclusions:

  • SFRP5 recombinant protein exhibits a protective effect against ISO-induced heart failure in mice.
  • SFRP5 may exert its protective effects by inhibiting the Wnt5A/JNK signaling pathway.
  • SFRP5's ability to reduce oxidative stress and inflammation suggests its potential as a therapeutic target for heart failure.

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