Evidence map›Paper›PMID 27274621›Full record

ReviewMediators of inflammation2016

Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations.

M Neri, I Riezzo, C Pomara, S Schiavone, E Turillazzi

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Nandrolone Decanoate: Use, Abuse and Side Effects.Medicina (Kaunas, Lithuania) · 2020
    Pooled it
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  9. LILRA5Frontiers in cellular and infection microbiology · 2025
    Article
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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

5 authors at 1 institution in 1 country.

M NeriInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
I RiezzoInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
C PomaraInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
S SchiavoneInstitute of Pharmacology, Department of Clinical and Experimental Medicine, University of Foggia, Via L. Pinto 1, 71100 Foggia, Italy.
E TurillazziInstitute of Forensic Pathology, Department of Clinical and Experimental Medicine, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial depression in sepsis is common, and it is associated with higher mortality. In recent years, the hypothesis that the myocardial dysfunction during sepsis could be mediated by ischemia related to decreased coronary blood flow waned and a complex mechanism was invoked to explain cardiac dysfunction in sepsis. Oxidative stress unbalance is thought to play a critical role in the pathogenesis of cardiac impairment in septic patients.

aimIn this paper, we review the current literature regarding the pathophysiology of cardiac dysfunction in sepsis, focusing on the possible role of oxidative-nitrosative stress unbalance and mitochondria dysfunction. We discuss these mechanisms within the broad scenario of cardiac involvement in sepsis.

conclusionsFindings from the current literature broaden our understanding of the role of oxidative and nitrosative stress unbalance in the pathophysiology of cardiac dysfunction in sepsis, thus contributing to the establishment of a relationship between these settings and the occurrence of oxidative stress. The complex pathogenesis of septic cardiac failure may explain why, despite the therapeutic strategies, sepsis remains a big clinical challenge for effectively managing the disease to minimize mortality, leading to consideration of the potential therapeutic effects of antioxidant agents.

Indexed as

AnimalsAutopsyCardiomyopathiesHumansOxidative StressSepsisStress, Physiological

Identifiers

PMID27274621
PMCPMC4870364
OpenAlexW2346389387

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.