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The role of NETosis in heart failure.
Sawa Kostin1, Florian Krizanic2, Theodoros Kelesidis3
1Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Neuruppin, Germany. Costin.Sava@mhb-fontane.de.
Heart Failure Reviews
|July 29, 2024
Summary
Neutrophil extracellular traps (NETs) contribute to heart failure (HF) pathogenesis through NETosis, a programmed cell death. Inhibiting NETosis markers like MPO, NE, and PAD4 shows promise in treating HF and related cardiac conditions.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathophysiology
Background:
- Heart failure (HF) is characterized by myocardial remodeling and chronic inflammation.
- Neutrophil extracellular traps (NETs) are crucial in immune defense and implicated in noninfectious diseases.
- NETosis, a form of neutrophil cell death, occurs in cardiac conditions but its role in HF pathogenesis is unclear.
Purpose of the Study:
- To review the mechanisms and markers of NETosis in the context of heart failure.
- To explore the potential of targeting NETosis pathways for HF therapy.
Main Methods:
- Analysis of mechanisms and markers of NETosis, focusing on myeloperoxidase (MPO), elastase (NE), and peptidylarginine deiminase 4 (PAD4).
- Review of genetic and pharmacological studies investigating the efficacy of NETosis inhibitors.
Main Results:
- NETosis is implicated in aggravating inflammation in cardiac conditions like myocardial infarction, myocarditis, and cardiomyopathies.
- Inhibitors of MPO, NE, and PAD4 demonstrate efficacy in preclinical models of adverse cardiac remodeling and HF development.
- NETosis markers are key to understanding HF pathophysiology.
Conclusions:
- NETosis is a significant contributor to heart failure pathogenesis.
- Targeting NETosis pathways, particularly MPO, NE, and PAD4, offers a promising therapeutic strategy for HF and associated cardiovascular diseases.
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