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Vascular Endothelial Growth Factor B Modulates Cardiac Functions via Ferroptosis Pathways in Post-Myocardial

Sai Manasa Varanasi1, Ankit Sabharwal2,3,4, Shreyartha Mukherjee5

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Vascular endothelial growth factor B (VEGFB) protects heart cells from damage after myocardial infarction (MI) by reducing cell death pathways like ferroptosis. Neuropilin-1 (NRP1) is crucial for this protective effect, highlighting VEGFB-NRP1 signaling as a potential therapy for ischemic heart disease.

Keywords:
FerroptosisNeuropilin-1 (NRP1)cardiomyocyteshypoxia/ischemiamitochondrial dysfunctionmyocardial infarctionvascular endothelial growth factor B (VEGFB)zebrafish

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Regenerative Medicine

Background:

  • Myocardial infarction (MI) is a major cause of death globally, with limited cardioprotective treatments.
  • Vascular endothelial growth factor B (VEGFB) shows therapeutic promise for MI.
  • The role of its co-receptor, Neuropilin-1 (NRP1), in cardiomyocyte survival during ischemia is unclear.

Purpose of the Study:

  • To investigate the role of VEGFB-NRP1 signaling in cardiomyocyte survival under ischemic stress.
  • To explore the therapeutic potential of VEGFB in a zebrafish model of cardiac injury and in vitro cardiomyocyte models.

Main Methods:

  • Utilized an in vivo zebrafish model of cardiac injury.
  • Employed in vitro hypoxia models using cardiomyocytes (CMs).
  • Performed gene knockdown (NRP1) and overexpression (VEGFB) experiments.
  • Conducted transcriptome analysis to identify gene expression changes.

Main Results:

  • VEGFB overexpression protected against ischemic injury and promoted cardiac regeneration in zebrafish.
  • VEGFB enhanced CM viability by reducing reactive oxygen species (ROS) and ferroptosis, preserving mitochondrial integrity.
  • NRP1 knockdown negated VEGFB's protective effects, confirming NRP1's essential role.
  • VEGFB activated anti-apoptotic and anti-ferroptosis gene programs in CMs under hypoxic stress.

Conclusions:

  • VEGFB-NRP1 signaling is critical for cardiomyocyte survival during ischemic stress.
  • VEGFB mitigates cell death pathways, including ferroptosis, in response to cardiac injury.
  • VEGFB represents a promising therapeutic target for treating ischemic heart disease and promoting cardiac repair.