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Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

478
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
478

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Related Experiment Video

Updated: Feb 26, 2026

A Microscopic 2,3,5-Triphenyltetrazolium Chloride Assay for Accurate and Reliable Analysis of Myocardial Injury
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PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury.

Jiawei Wu1,2, Shule Zhang1,3, Ruofan Du1,3

  • 1State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, P. R. China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 25, 2026
PubMed
Summary

Platelet activating factor (PAF) drives neutrophil extracellular trap (NET) formation, worsening myocardial ischemia-reperfusion (MI/R) injury. Dapagliflozin inhibits this process, offering a potential therapeutic strategy for MI/R injury.

Keywords:
NETosisdapagliflozinmyocardial ischemia‐reperfusion injuryplatelet activating factor

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Metabolic Signaling

Background:

  • Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem.
  • The interplay between metabolic and inflammatory pathways in MI/R injury is not fully understood.

Purpose of the Study:

  • To investigate the role of neutrophil extracellular traps (NETs) and platelet activating factor (PAF) in MI/R injury.
  • To identify therapeutic targets for mitigating MI/R injury.

Main Methods:

  • Verified NETosis as a key driver of MI/R injury.
  • Demonstrated PAF secreted by cardiomyocytes induces NETosis via PLA2G6 and gasdermin D (GSDMD).
  • Evaluated dapagliflozin as a NETosis inhibitor targeting lipocalin-2 (LCN2) in a SGLT2-independent manner.

Main Results:

  • Inhibiting NETs or PAF synthesis significantly reduced MI/R injury in mice.
  • Dapagliflozin protected mice from MI/R injury.
  • Elevated serum PAF correlated with NETosis and myocardial injury in patients; dapagliflozin use was associated with attenuated injury.

Conclusions:

  • PAF acts as a danger signal initiating NETosis in early MI/R injury.
  • Targeting the PAF-NETosis pathway with agents like dapagliflozin or LCN2 inhibitors shows therapeutic potential for MI/R injury.