Evidence map›Paper›PMID 34440901›Full record

ArticleCells2021

Adenine Nucleotide Translocase 1 Expression Modulates the Immune Response in Ischemic Hearts.

Fatih Yergöz, Julian Friebel, Nicolle Kränkel, Ursula Rauch-Kroehnert, Heinz-Peter Schultheiss, Ulf Landmesser, Andrea Dörner

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
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

7 authors at 2 institutions in 1 country.

Fatih YergözDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.ORCID 0000-0002-9709-8563
Julian FriebelDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.
Nicolle KränkelDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.ORCID 0000-0002-9363-1770
Ursula Rauch-KroehnertDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.
Heinz-Peter SchultheissInstitute for Cardiac Diagnostics and Therapy (IKDT), 12203 Berlin, Germany.
Ulf LandmesserDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.
Andrea DörnerDepartment of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.ORCID 0000-0003-1398-1779
Humboldt-Universität zu Berlin · DECS Diagnostics · DE

Funding

German Centre for Cardiovascular Research FKZ 81Z0100202
6 · The paper itself

Abstract

Adenine nucleotide translocase 1 (ANT1) transfers ATP and ADP over the mitochondrial inner membrane and thus supplies the cell with energy. This study analyzed the role of ANT1 in the immune response of ischemic heart tissue. Ischemic ANT1 overexpressing hearts experienced a shift toward an anti-inflammatory immune response. The shift was characterized by low interleukin (IL)-1β expression and M1 macrophage infiltration, whereas M2 macrophage infiltration and levels of IL-10, IL-4, and transforming growth factor (TGFβ) were increased. The modulated immune response correlated with high mitochondrial integrity, reduced oxidative stress, low left ventricular end-diastolic heart pressure, and a high survival rate. Isolated ANT1-transgenic (ANT1-TG) cardiomyocytes expressed low levels of pro-inflammatory cytokines such as IL-1α, tumor necrosis factor α, and TGFβ. However, they showed increased expression and cellular release of anti-inflammatory immunomodulators such as vascular endothelial growth factor. The secretome from ANT1-TG cardiomyocytes initiated stress resistance when applied to ischemic wild-type cardiomyocytes and endothelial cells. It additionally prevented macrophages from expressing pro-inflammatory cytokines. Additionally, ANT1 expression correlated with genes that are related to cytokine and growth factor pathways in hearts of patients with ischemic cardiomyopathy. In conclusion, ANT1-TG cardiomyocytes secrete soluble factors that influence ischemic cardiac cells and initiate an anti-inflammatory immune response in ischemic hearts.

Indexed as

AnimalsBlotting, WesternCardiomyopathiesCells, CulturedImmunohistochemistryMaleMembrane Potential, MitochondrialMitochondria, HeartMitochondrial ADP, ATP TranslocasesMitochondrial MembranesMyocardial InfarctionRatsReal-Time Polymerase Chain ReactionMitochondrial ADP, ATP Translocasesadenine nucleotide translocasecytokineimmune responseischemic cardiomyopathymacrophagesmitochondriamyocardial infarction

Identifiers

PMID34440901
PMCPMC8393693
OpenAlexW3194808107

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.