Evidence mapPaperPMID 27923790Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2017

Dynamin-related protein 1 mediates low glucose-induced endothelial dysfunction in human arterioles.

Michael J Tanner, Jingli Wang, Rong Ying, Tisha B Suboc, Mobin Malik, Allison Couillard, Amberly Branum, Venkata Puppala, Michael E Widlansky

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Review
  3. Impaired endothelial function contributes to cardiac dysfunction: role of mitochondrial dynamics.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Mitochondrial division inhibitor 1 (mdivi-1) increases oxidative capacity and contractile stress generated by engineered skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Mitochondrial regulation of diabetic vascular disease: an emerging opportunity.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  17. Article
  18. Statistical considerations in reporting cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  19. Review
  20. To mdivi-1 or not to mdivi-1: Is that the question?Developmental neurobiology · 2017
    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

9 authors at 1 institution in 1 country.

Michael J TannerDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Jingli WangDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Rong YingDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Tisha B SubocDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Mobin MalikDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Allison CouillardDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Amberly BranumDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Venkata PuppalaDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Michael E WidlanskyDivision of Cardiovascular Medicine, Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin mwidlans@mcw.edu.
Medical College of Wisconsin · US

Funding

NHLBI NIH HHS K23 HL089326NHLBI NIH HHS R01 HL125409NHLBI NIH HHS R01 HL128240
6 · The paper itself

Abstract

Intensive glycemic regulation has resulted in an increased incidence of hypoglycemia. Hypoglycemic burden correlates with adverse cardiovascular complications and contributes acutely and chronically to endothelial dysfunction. Prior data indicate that mitochondrial dysfunction contributes to hypoglycemia-induced endothelial dysfunction, but the mechanisms behind this linkage remain unknown. We attempt to determine whether clinically relevant low-glucose (LG) exposures acutely induce endothelial dysfunction through activation of the mitochondrial fission process. Characterization of mitochondrial morphology was carried out in cultured endothelial cells by using confocal microscopy. Isolated human arterioles were used to explore the effect LG-induced mitochondrial fission has on the formation of detrimental reactive oxygen species (ROS), bioavailability of nitric oxide (NO), and endothelial-dependent vascular relaxation. Fluorescence microscopy was employed to visualize changes in mitochondrial ROS and NO levels and videomicroscopy applied to measure vasodilation response. Pharmacological disruption of the profission protein Drp1 with Mdivi-1 during LG exposure reduced mitochondrial fragmentation among vascular endothelial cells (LG: 0.469; LG+Mdivi-1: 0.276;

Indexed as

ArteriolesAdultAgedDynaminsEndothelium, VascularEnergy MetabolismFemaleGene Knockdown TechniquesGlucoseGTP PhosphohydrolasesHumansHuman Umbilical Vein Endothelial CellsMaleMembrane Potential, MitochondrialMicrotubule-Associated ProteinsMiddle Aged3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneDNM1L protein, humanDynaminsGlucoseGTP PhosphohydrolasesMicrotubule-Associated ProteinsMitochondrial ProteinsNitric OxideQuinazolinonesReactive Oxygen SpeciesRNA, Small Interferingendothelial dysfunctionglucosemitochondrianitric oxidevasodilation

Identifiers

PMID27923790
PMCPMC5402007
OpenAlexW2560452919

What Socratic 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 Socratic graph.