Evidence map›Paper›PMID 28067713›Full record

ArticleCritical care medicine2017

Widespread Down-Regulation of Cardiac Mitochondrial and Sarcomeric Genes in Patients With Sepsis.

Scot J Matkovich, Belal Al Khiami, Igor R Efimov, Sarah Evans, Justin Vader, Ashwin Jain, Bernard H Brownstein, Richard S Hotchkiss, Douglas L Mann

Abstract read
In one paragraph

Article in Critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

76 citing papers in PubMed, 117 citations in OpenAlex.

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  20. Utilizing omics technologies in the investigation of sepsis-induced cardiomyopathy.International journal of cardiology. Heart & vasculature · 2024
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Scot J Matkovich1Center for Pharmacogenomics, John T. Milliken Department of Medicine, Washington University School of Medicine, St. Louis, MO. 2Center for Cardiovascular Research, Cardiovascular Division, John T. Milliken Department of Medicine, Washington University School of Medicine, St. Louis, MO. 3Division of Cardiovascular Medicine, Sulpizio Cardiovascular Center, University of California, San Diego, CA. 4Department of Biomedical Engineering, George Washington University, Washington, DC. 5Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO.
Belal Al Khiami
Igor R Efimov
Sarah Evans
Justin Vader
Ashwin Jain
Bernard H Brownstein
Richard S Hotchkiss
Douglas L Mann
George Washington University · USWashington University in St. Louis · US

Funding

Exploration of Arrhythmogenic Triggers and Substrates in Heart FailureR01HL126802 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI EFIMOV, IGOR R, GORELIK, JULIA · 2016 to 2019
$2.8M
PREVENTION OF APOPTOTIC CELL DEATH IN SEPSIS BY BCL-2R01GM044118 · NIGMS · WASHINGTON UNIVERSITY · PI HOTCHKISS, RICHARD SAMUEL · 1992 to 2017
$2.7M
ARRHYTHMOGENIC REMODELING IN HUMAN HEART FAILURER01HL114395 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2012 to 2015
$2.1M
Cardiac Inflammation in Resuscitated Hemorrhagic ShockR01HL073017 · NHLBI · WASHINGTON UNIVERSITY · PI MANN, DOUGLAS L · 2005 to 2008
$1.4M
CAUSE AND CONSEQUENCE OF TNF OVEREXPRESSION IN THE HEARTR01HL058081 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MANN, DOUGLAS LOWELL · 1998 to 2007
$1.4M
Cytoprotective Cytokine Signaling and Reperfusion InjuryR01HL089543 · NHLBI · WASHINGTON UNIVERSITY · PI MANN, DOUGLAS L · 2009 to 2010
$779k
NHLBI NIH HHS R01 HL058081NHLBI NIH HHS R01 HL073017NHLBI NIH HHS R01 HL089543NHLBI NIH HHS R01 HL114395NHLBI NIH HHS R01 HL126802NIGMS NIH HHS R01 GM044118
6 · The paper itself

Abstract

objectivesThe mechanism(s) for septic cardiomyopathy in humans is not known. To address this, we measured messenger RNA alterations in hearts from patients who died from systemic sepsis, in comparison to changed messenger RNA expression in nonfailing and failing human hearts.

designIdentification of genes with altered abundance in septic cardiomyopathy, ischemic heart disease, or dilated cardiomyopathy, in comparison to nonfailing hearts.

settingICUs at Barnes-Jewish Hospital, St. Louis, MO. PATIENTS: Twenty sepsis patients, 11 ischemic heart disease, nine dilated cardiomyopathy, and 11 nonfailing donors.

interventionsNone other than those performed as part of patient care. MEASUREMENTS AND MAIN

resultsMessenger RNA expression levels for 198 mitochondrially localized energy production components, including Krebs cycle and electron transport genes, decreased by 43% ± 5% (mean ± SD). Messenger RNAs for nine genes responsible for sarcomere contraction and excitation-contraction coupling decreased by 43% ± 4% in septic hearts. Surprisingly, the alterations in messenger RNA levels in septic cardiomyopathy were both distinct from and more profound than changes in messenger RNA levels in the hearts of patients with end-stage heart failure.

conclusionsThe expression profile of messenger RNAs in the heart of septic patients reveals striking decreases in expression levels of messenger RNAs that encode proteins involved in cardiac energy production and cardiac contractility and is distinct from that observed in patients with heart failure. Although speculative, the global nature of the decreases in messenger RNA expression for genes involved in cardiac energy production and contractility suggests that these changes may represent a short-term adaptive response of the heart in response to acute change in cardiovascular homeostasis.

Indexed as

Down-RegulationTranscriptomeAdultAgedAged, 80 and overCardiomyopathiesCardiomyopathy, DilatedCitric Acid CycleElectron TransportFemaleHumansMaleMiddle AgedMitochondria, HeartMyocardial IschemiaRNA, MessengerRNA, Messenger

Identifiers

PMID28067713
PMCPMC5315660
OpenAlexW2569704268

What OpenQuestion holds

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LicenceTDM
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.