Evidence map›Paper›PMID 20227109›Full record

ArticleCell calcium2010

TNF-alpha and IL-1beta increase Ca2+ leak from the sarcoplasmic reticulum and susceptibility to arrhythmia in rat ventricular myocytes.

David J Duncan, Zhaokang Yang, Philip M Hopkins, Derek S Steele, Simon M Harrison

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Cell calcium, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05202938 (Energy MEtabolism of Septic Heart.), which is not on this map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
3.6field-weighted citation impact, top 6% 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.

NCT05202938 unknown statusnot on this mapstarted 2022, after this paper: background citation

Energy MEtabolism of Septic Heart.

TypeobservationalSponsorCentre de recherche du Centre hospitalier universitaire de SherbrookeRan2022 to 2024Enrolled32ConditionsSeptic Shock, Chronic Heart FailureArmsultrasound cardiography, FDG PET scan, Palmitate PET scan, Acetate PET scan, Blood sampling
3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 152 citations in OpenAlex.

  1. Review
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  3. Review
  4. Association Between Myocardial Dysfunction and Septic Shock.International journal of molecular sciences · 2026
    Review
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29 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 1 institution in 1 country.

David J DuncanMultidisciplinary Cardiovascular Research Centre, Institute of Membrane and Systems Biology, University of Leeds, Leeds LS29JT, UK.
Zhaokang Yang
Philip M Hopkins
Derek S Steele
Simon M Harrison
University of Leeds · GB

Funding

British Heart Foundation
6 · The paper itself

Abstract

Sepsis is associated with ventricular dysfunction and increased incidence of atrial and ventricular arrhythmia however the underlying pro-arrhythmic mechanisms are unknown. Serum levels of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) are elevated during sepsis and affect Ca2+ regulation. We investigated whether pro-inflammatory cytokines disrupt cellular Ca2+ cycling leading to reduced contractility, but also increase the probability of pro-arrhythmic spontaneous Ca2+ release from the sarcoplasmic reticulum (SR). Isolated rat ventricular myocytes were exposed to TNF-alpha (0.05 ng ml(-1)) and IL-1beta (2 ng ml(-1)) for 3 hr and then loaded with fura-2 or fluo-3 to record the intracellular Ca2+ concentration ([Ca2+](i)). Cytokine treatment decreased the amplitude of the spatially averaged Ca2+ transient and the associated contraction, induced asynchronous Ca2+ release during electrical stimulation, increased the frequency of localized Ca2+ release events, decreased the SR Ca2+ content and increased the frequency of spontaneous Ca2+ waves at any given cytoplasmic Ca2+. These data suggest that TNF-alpha and IL-1beta increase the SR Ca2+ leak from the SR, which contributes to the depressed Ca2+ transient and contractility. Increased susceptibility to spontaneous SR Ca2+ release may contribute to arrhythmias in sepsis as the resulting Ca2+ extrusion via NCX is electrogenic, leading to cell depolarisation.

Indexed as

AnimalsArrhythmias, CardiacCalcium SignalingCells, CulturedDisease SusceptibilityHeart VentriclesInterleukin-1betaMaleMuscle CellsMyocardial ContractionRatsRats, WistarSarcoplasmic ReticulumSepsisTumor Necrosis Factor-alphaInterleukin-1betaTumor Necrosis Factor-alpha

Identifiers

PMID20227109
PMCPMC2877880
OpenAlexW2078575750

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.