Evidence map›Paper›PMID 26142467›Full record

ReviewEuropean heart journal2015

Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications.

Thomas Münzel, Tommaso Gori, John F Keaney, Christoph Maack, Andreas Daiber

Open access · bronzeAbstract readReview
In one paragraph

Review in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 2 pooled it
22.2field-weighted citation impact, top 1% of its field
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

168 citing papers in PubMed, 2 syntheses or guidelines pooled it, 377 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Dietary Nitrate Increases VOJournal of cardiac failure · 2018
    Trial
  5. Trial
  6. β-Blockers and ivabradine differentially affect cardiopulmonary function and left ventricular filling index.Clinical research in cardiology : official journal of the German Cardiac Society · 2016
    Trial
  7. Review
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  20. Peroxynitrite regulates ER stress-mediated CaJournal of translational medicine · 2025
    Article

108 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Thomas Münzel2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany tmuenzel@uni-mainz.de.
Tommaso Gori2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany.
John F KeaneyUniversity of Massachusetts Medical School, Worcester, MA, USA.
Christoph MaackKlinik für Innere Medizin III Universitätsklinikum des Saarlandes, Homburg/Saar, Germany.
Andreas Daiber2nd Medical Clinic, Department of Cardiology, Medical Center of the Johannes Gutenberg University, Langenbeckstrasse 1, Mainz 55131, Germany.
Johannes Gutenberg University Mainz · DEUniversitätsklinikum des Saarlandes · DEUniversity of Massachusetts Chan Medical School · US

Funding

Nox4 and Vascular HomeostasisR01HL098407 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2010 to 2017
$3.8M
NHLBI NIH HHS R01 HL098407
6 · The paper itself

Abstract

Systolic and diastolic myocardial dysfunction has been demonstrated to be associated with an activation of the circulating and local renin-angiotensin-aldosterone system (RAAS), and with a subsequent inappropriately increased production of reactive oxygen species (ROS). While, at low concentrations, ROS modulate important physiological functions through changes in cellular signalling and gene expression, overproduction of ROS may adversely alter cardiac mechanics, leading to further worsening of systolic and diastolic function. In addition, vascular endothelial dysfunction due to uncoupling of the nitric oxide synthase, activation of vascular and phagocytic membrane oxidases or mitochondrial oxidative stress may lead to increased vascular stiffness, further compromising cardiac performance in afterload-dependent hearts. In the present review, we address the potential role of ROS in the pathophysiology of myocardial and vascular dysfunction in heart failure (HF) and their therapeutic targeting. We discuss possible mechanisms underlying the failure of antioxidant vitamins in improving patients' prognosis, the impact of angiotensin-converting enzyme inhibitors or AT1 receptor blockers on oxidative stress, and the mechanism of the benefit of combination of hydralazine/isosorbide dinitrate. Further, we provide evidence supporting the existence of differences in the pathophysiology of HF with preserved vs. reduced ejection fraction and whether targeting mitochondrial ROS might be a particularly interesting therapeutic option for patients with preserved ejection fraction.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAntioxidantsCardiovascular SystemDrug Therapy, CombinationExercise TherapyHeart Failure, DiastolicHeart Failure, SystolicHumansHydralazineMitochondriaNADPH OxidasesNitratesNitric OxideNitric Oxide SynthaseOxidative StressPhosphodiesterase InhibitorsAngiotensin-Converting Enzyme InhibitorsAntioxidantsHydralazineNADPH OxidasesNitratesNitric OxideNitric Oxide SynthasePhosphodiesterase InhibitorsReactive Oxygen SpeciesVitaminsXanthine Oxidase

Identifiers

PMID26142467
PMCPMC7959410
OpenAlexW2119221698

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.