Evidence map›Paper›PMID 25380814›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Downregulation of adenine nucleotide translocator 1 exacerbates tumor necrosis factor-α-mediated cardiac inflammatory responses.

Shi Pan, Nadan Wang, Sara Bisetto, Bing Yi, Shey-Shing Sheu

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Bnip3 regulates airway smooth muscle cell focal adhesion and proliferation.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  8. Article
  9. Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  10. Article
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.

Shi PanDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
Nadan WangDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
Sara BisettoDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
Bing YiDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
Shey-Shing SheuDepartment of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania shey-shing.sheu@jefferson.edu.
Thomas Jefferson University · US

Funding

Ca2+ and ROS Crosstalk Signaling in Cardiac MitochondriaR01HL093671 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 2010 to 2023
$5.1M
Vevo 2100 ultrasound scannerS10OD010408 · OD · THOMAS JEFFERSON UNIVERSITY · PI FORSBERG, FLEMMING · 2012 to 2012
$525k
ADP: A Master Regulator for Bioenergetics and Ca2+/ROS Signaling in HeartR21HL110371 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI SHEU, SHEY-SHING · 2011 to 2012
$426k
NHLBI NIH HHS HL093671NHLBI NIH HHS HL110371NHLBI NIH HHS R01 HL093671NIH HHS S10 OD010408
6 · The paper itself

Abstract

Inflammation contributes significantly to cardiac dysfunction. Although the initial phase of inflammation is essential for repair and healing, excessive proinflammatory cytokines are detrimental to the heart. We found that adenine nucleotide translocator isoform-1 (ANT1) protein levels were significantly decreased in the inflamed heart of C57BL/6 mice following cecal ligation and puncture. To understand the molecular mechanisms involved, we performed small-interfering RNA-mediated knockdown of ANT1 and studied tumor necrosis factor-α (TNFα)-induced inflammatory responses in myocardium-derived H9c2 cells and cardiomyocytes. ANT1 knockdown significantly increased swollen mitochondria and mitochondrial reactive oxygen species, concomitant with increased TNFα-induced NF-κB reporter gene activity and interleukin-6 and TNFα expression. A mitochondrial-targeted antioxidant mito-TEMPO attenuated TNFα-induced mitochondrial reactive oxygen species, NF-κB reporter gene activity, and cytokine expression in ANT1 knockdown cells. Interestingly, TNFα or lipopolysaccharide (LPS) treatment significantly decreased ANT1 protein levels, suggesting a feed-forward regulation of proinflammatory cytokine expression activated by ANT1 downregulation. These data suggest that ANT1 downregulation contributes to cardiac inflammation post-cecal ligation and puncture. Preventing ANT1 downregulation could provide a novel molecular target to temper cardiac inflammation.

Indexed as

Adenine Nucleotide Translocator 1AnimalsCell LineDisease Models, AnimalDown-RegulationGenes, ReporterInflammationInflammation MediatorsInterleukin-6LipopolysaccharidesMaleMembrane Potential, MitochondrialMice, Inbred C57BLMitochondria, HeartMitochondrial SwellingMyocytes, CardiacAdenine Nucleotide Translocator 1Inflammation MediatorsInterleukin-6interleukin-6, mouseLipopolysaccharidesNF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alphaadenine nucleotide translocatorcytokineinflammationsepsis

Identifiers

PMID25380814
PMCPMC4281676
OpenAlexW1963699887

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.