Evidence map›Paper›PMID 39073665›Full record

ReviewHeart failure reviews2024

The role of NETosis in heart failure.

Sawa Kostin, Florian Krizanic, Theodoros Kelesidis, Nikolaos Pagonas

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Heart failure reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Sawa KostinFaculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Neuruppin, Germany. Costin.Sava@mhb-fontane.de.ORCID 0000-0002-1594-9476
Florian KrizanicDepartment of Internal Medicine and Cardiology, Medical School Theodor Fontane, University Hospital Ruppin-Brandenburg, Neuruppin, Germany.
Theodoros KelesidisUniversity of Texas Southwestern Medical Center, Dallas, USA.
Nikolaos PagonasFaculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Neuruppin, Germany.

Funding

Targeting early instigators of vascular inflammation to prevent and/or delay vascular aging in chronic treated HIVR01AG059502 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI KELESIDIS, THEODOROS · 2018 to 2022
$2.0M
NIA NIH HHS R01 AG059502
6 · The paper itself

Abstract

The hallmark of heart failure (HF) is structural myocardial remodeling including cardiomyocyte hypertrophy, fibrosis, cardiomyocyte cell death, and a low-grade aseptic inflammation. The initiation and maintenance of persistent chronic low-grade inflammation in HF are not fully understood. Oxidative stress-mediated neutrophil extracellular traps (NETs) are the main immune defense mechanism against external bacterial infections. Furthermore, NETs play important roles in noninfectious diseases. In the settings of myocardial infarction, myocarditis, or cardiomyopathies, neutrophils infiltrate the cardiac tissue and undergo NETosis that further aggravate the inflammation. A number of stimuli may cause NETosis that is a form of programmed cell death of neutrophils that is different from apoptosis of these cells. Whether NETosis is directly involved in the pathogenesis and development of HF is still unclear. In this review, we analyzed the mechanisms and markers of NETosis, especially placing the accent on the activation of the neutrophil-specific myeloperoxidase (MPO), elastase (NE), and peptidylarginine deiminase 4 (PAD4). These conclusions are supported by the recent genetic and pharmacological studies which demonstrated that MPO, NE, and PAD4 inhibitors are effective at least in the settings of post-myocardial infarction adverse remodeling, cardiac valve diseases, cardiomyopathies, and decompensated left ventricular hypertrophy whose deterioration can lead to HF. This is essential for understanding NETosis as a contributor to pathophysiology of HF and developments of new therapies of HF.

Indexed as

Extracellular TrapsHeart FailureNeutrophilsHumansInflammationOxidative StressVentricular RemodelingHeart failureInflammationNETosisNeutrophils

Identifiers

PMID39073665
PMCPMC12066148

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.