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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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Related Experiment Video

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ZLY032 mediated activation of Notch1/Hes1 signaling inhibits cardiomyocyte ferroptosis to protect against myocardial

Hao-Dong Li1, Dong-Ping Liu1, Man-Yu Gong1

  • 1Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.

Biochemical Pharmacology
|June 11, 2025
PubMed
Summary

Notch1 activation protects the heart by inhibiting ferroptosis, a cell death pathway implicated in myocardial ischemia/reperfusion (I/R) injury. The compound ZLY032 enhances this protection via the PPARδ-Notch1-GPX4 pathway.

Keywords:
FerroptosisGPX4Myocardial ischemia/reperfusion injuryNotch1PPARδZLY032

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Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Pharmacology

Background:

  • Myocardial ischemia/reperfusion (I/R) injury is a major cause of mortality.
  • Ferroptosis, a form of regulated cell death, plays a significant role in I/R injury.
  • The Notch1 signaling pathway is known to have protective effects in the heart.

Purpose of the Study:

  • To investigate whether Notch1 activation inhibits cardiomyocyte ferroptosis and elucidate the underlying mechanisms.
  • To evaluate the cardioprotective effects of ZLY032, a PPARδ agonist, in myocardial I/R injury.

Main Methods:

  • Activating the Notch signaling pathway in cardiomyocytes subjected to I/R.
  • Treating animal models of myocardial I/R injury with ZLY032.
  • Assessing levels of lipid peroxidation, oxidative stress, and ferroptosis markers.
  • Investigating the interaction between Notch intracellular domain (NICD) and GPX4.

Main Results:

  • Notch1 activation suppressed cardiomyocyte ferroptosis by reducing lipid peroxidation and oxidative stress.
  • ZLY032 treatment alleviated cardiac dysfunction, reduced infarct size, and mitigated ferroptosis in I/R injury models.
  • Notch1 activation increased GPX4 expression, and NICD inhibited GPX4 degradation.
  • ZLY032 activated PPARδ, which in turn activated Notch1 signaling.

Conclusions:

  • Notch1 inhibits ferroptosis in cardiomyocytes by stabilizing GPX4 protein.
  • ZLY032 demonstrates cardioprotective effects against I/R injury through the PPARδ-Notch1-GPX4 axis.
  • ZLY032 is a potential therapeutic agent for myocardial I/R injury.