Evidence map›Paper›PMID 25530817›Full record

ArticleCellular and molecular bioengineering2014

Fluid Mechanical Forces and Endothelial Mitochondria: A Bioengineering Perspective.

Christopher G Scheitlin, Devi M Nair, Juan A Crestanello, Jay L Zweier, B Rita Alevriadou

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2014. 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
1.1field-weighted citation impact, top 24% 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, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Modulation of the mitochondrial CaPhysiological reports · 2023
    Article
  4. Article
  5. The mitochondrial CaScientific reports · 2022
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Shear stress augments mitochondrial ATP generation that triggers ATP release and CaAmerican journal of physiology. Heart and circulatory physiology · 2018
    Article
  16. Article
  17. Mitochondrial CaJournal of the Royal Society, Interface · 2017
    Review
  18. Melatonin, mitochondria and hypertension.Cellular and molecular life sciences : CMLS · 2017
    Review
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Christopher G ScheitlinLaboratory of Vascular Mechanotransduction & Oxidative Stress, Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210 ; Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210.
Devi M NairLaboratory of Vascular Mechanotransduction & Oxidative Stress, Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210 ; Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210.
Juan A CrestanelloDavis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210 ; Department of Surgery, Division of Cardiac Surgery, Wexner Medical Center, The Ohio State University, Columbus, OH 43210.
Jay L ZweierDavis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210 ; Department of Internal Medicine, Division of Cardiovascular Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH 43210.
B Rita AlevriadouLaboratory of Vascular Mechanotransduction & Oxidative Stress, Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210 ; Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210 ; Department of Internal Medicine, Division of Cardiovascular Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH 43210.
The Ohio State University · US

Funding

Emerging Functions of Mitochondrial Fission in Postischemic Endothelial CellsR21HL106392 · NHLBI · OHIO STATE UNIVERSITY · PI ALEVRIADOU, BARBARA RITA · 2011 to 2012
$423k
NHLBI NIH HHS R21 HL106392
6 · The paper itself

Abstract

Endothelial cell dysfunction is the hallmark of every cardiovascular disease/condition, including atherosclerosis and ischemia/reperfusion injury. Fluid shear stress acting on the vascular endothelium is known to regulate cell homeostasis. Altered hemodynamics is thought to play a causative role in endothelial dysfunction. The dysfunction is associated with/preceded by mitochondrial oxidative stress. Studies by our group and others have shown that the form and/or function of the mitochondrial network are affected when endothelial cells are exposed to shear stress in the absence or presence of additional physicochemical stimuli. The present review will summarize the current knowledge on the interconnections among intracellular Ca

Indexed as

autophagycardiovascular diseaseendothelial dysfunctionischemia/reperfusionmitochondrial fissionmitophagynitric oxideoxidative stressreactive oxygen speciesShear stress

Identifiers

PMID25530817
PMCPMC4270056
OpenAlexW1970724906

What OpenQuestion holds

Textmetadata
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.