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June 10, 2020Antioxidants and Redox SignalingOpen Access

Preclinical data indicate that metabolic imbalances post-AMI contribute to heart failure through sustaining local recruitment of inflammatory leukocytes, oxidative stress, and cardiomyocyte death, highlighting neutrophil-derived myeloperoxidase (MPO) as a potential therapeutic target.

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Why the study?

Reperfusion post-AMI triggers inflammatory and oxidative damage contributing to heart failure, but therapeutic anti-inflammatory and antioxidant agents successful in preclinical studies have failed in clinical trials.

Design

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Authors

MKMary El KazziBCBelal ChamiJDJoanne M. Dennis

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Overview

MPO inhibition remains investigational post-AMI; leaves open whether neutrophil-derived myeloperoxidase prevents clinical heart failure.

Key Points

Key points are not available for this paper at this time.

Cite This Study

Kazzi et al. (2020) studied this question.

synapsesocial.com/papers/6a7ff5cdcf96de1eb9c858b2https://doi.org/10.1089/ars.2019.7928
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Protective Effects of Therapeutic Neutrophil Depletion and Myeloperoxidase Inhibition on Left Ventricular Function and Remodeling in Myocardial Infarction2022 · 17 citations
  2. 2Myeloperoxidase as a Promising Therapeutic Target after Myocardial Infarction2024 · 15 citations
  3. 3Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities2019 · 228 citations
  4. 4Antioxidant Cardioprotection in Acute Myocardial Infarction: From Mechanisms to Therapeutic Strategies2025
  5. 5Cross-Talk Between Neutrophils and Macrophages Post-Myocardial Infarction: From Inflammatory Drivers to Therapeutic Targets2025 · 13 citations