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Related Experiment Video

Updated: May 10, 2025

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
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Protein-Like Polymers Targeting Keap1/Nrf2 as Therapeutics for Myocardial Infarction.

Joshua M Mesfin1, Kendal P Carrow2, Alexander Chen3

  • 1Shu Chien-Gene Lay Department of Bioengineering, Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, CA, 92037, USA.

Advanced Materials (Deerfield Beach, Fla.)
|April 25, 2025
PubMed
Summary
This summary is machine-generated.

A novel protein-like polymer (PLP) therapy targeting Keap1/Nrf2 interactions shows promise for treating myocardial infarction (MI). This innovative approach mitigates oxidative stress and inflammation, improving cardiac function post-MI.

Keywords:
biomaterialdrug deliverymyocardial infarctionpolymers

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Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Drug Discovery

Background:

  • Myocardial infarction (MI) causes oxidative stress and inflammation, often leading to heart failure (HF).
  • Current treatments lack efficacy in preventing adverse cardiac remodeling post-MI.
  • Targeting the Keap1/Nrf2 pathway offers a potential therapeutic strategy to combat MI-induced damage.

Purpose of the Study:

  • To develop and evaluate a novel Nrf2-mimetic protein-like polymer (PLP) as a therapeutic agent for myocardial infarction (MI).
  • To investigate the ability of Keap1-inhibiting PLPs (Keap1i-PLPs) to mitigate oxidative stress and inflammation following MI.
  • To assess the in vivo efficacy of Keap1i-PLPs in improving cardiac function and preventing adverse remodeling post-MI.

Main Methods:

  • Utilized a protein-like polymer (PLP) platform designed to mimic Nrf2 and inhibit the Keap1-Nrf2 interaction.
  • Conducted in vitro assays using primary cardiomyocytes to assess cytoprotection and Nrf2 activation.
  • Performed in vivo studies in a rat model of MI, administering Keap1i-PLPs intravenously to evaluate cardiac function and underlying mechanisms.

Main Results:

  • Keap1i-PLPs demonstrated potent cytoprotective effects against oxidative stress in cardiomyocytes via Nrf2 activation at sub-nanomolar concentrations.
  • A single intravenous dose of Keap1i-PLPs significantly improved cardiac function in rats post-MI.
  • Therapeutic benefits were attributed to immunomodulatory, anti-apoptotic, and angiogenic mechanisms.

Conclusions:

  • Keap1i-PLPs effectively disrupt the Keap1-Nrf2 protein-protein interaction following systemic administration.
  • This novel therapeutic strategy shows significant potential for treating myocardial infarction and other oxidative stress-related diseases.
  • The PLP platform offers a promising approach for developing therapeutics targeting intracellular protein-protein interactions.