Evidence map›Paper›PMID 29351466›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2018

Telomerase reverse transcriptase protects against angiotensin II-induced microvascular endothelial dysfunction.

Karima Ait-Aissa, Andrew O Kadlec, Joseph Hockenberry, David D Gutterman, Andreas M Beyer

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Endothelial TERT drives microvascular phenotype associated with coronary artery disease.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Autophagy, TERT, and mitochondrial dysfunction in hyperoxia.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Telomeres as Therapeutic Targets in Heart Disease.JACC. Basic to translational science · 2019
    Review
  20. Detrimental effects of chemotherapy on human coronary microvascular function.American journal of physiology. Heart and circulatory physiology · 2019
    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.

Karima Ait-AissaDepartment of Medicine, Cardiovascular Center, Medical College of Wisconsin , Milwaukee, Wisconsin.
Andrew O KadlecDepartment of Medicine, Cardiovascular Center, Medical College of Wisconsin , Milwaukee, Wisconsin.ORCID 0000-0003-2263-8622
Joseph HockenberryDepartment of Medicine, Cardiovascular Center, Medical College of Wisconsin , Milwaukee, Wisconsin.
David D GuttermanDepartment of Medicine, Cardiovascular Center, Medical College of Wisconsin , Milwaukee, Wisconsin.ORCID 0000-0003-2814-7867
Andreas M BeyerDepartment of Medicine, Cardiovascular Center, Medical College of Wisconsin , Milwaukee, Wisconsin.ORCID 0000-0001-9129-7492
Medical College of Wisconsin · US

Funding

Medical Scientist Training ProgramT32GM080202 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI BARBIERI, JOSEPH T, SALZMAN, NITA H · 2010 to 2024
$5.7M
Pivotal Role of Mitochondrial Telomerase in Regulation of Vascular Tone and Redox HomeostasisR01HL133029 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI BEYER, ANDREAS M · 2017 to 2021
$2.2M
Mechanism of Flow-Induced Dilation in the Human MicrocirculationR01HL113612 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2013 to 2016
$1.7M
NHLBI NIH HHS R01 HL113612NHLBI NIH HHS R01 HL133029NIGMS NIH HHS T32 GM080202
6 · The paper itself

Abstract

A rise in reactive oxygen species (ROS) may contribute to cardiovascular disease by reducing nitric oxide (NO) levels, leading to loss of NO's vasodilator and anti-inflammatory effects. Although primarily studied in larger conduit arteries, excess ROS release and a corresponding loss of NO also occur in smaller resistance arteries of the microcirculation, but the underlying mechanisms and therapeutic targets have not been fully characterized. We examined whether either of the two subunits of telomerase, telomerase reverse transcriptase (TERT) or telomerase RNA component (TERC), affect microvascular ROS production and peak vasodilation at baseline and in response to in vivo administration to angiotensin II (ANG II). We report that genetic loss of TERT [maximal dilation: 52.0 ± 6.1% with vehicle, 60.4 ± 12.9% with N

Indexed as

Angiotensin IIAnimalsCoronary VesselsEndothelium, VascularFemaleHydrogen PeroxideMaleMesenteric ArteriesMice, Inbred C57BLMice, KnockoutMicrovesselsNitric OxideRNATelomeraseVasodilationAngiotensin IIHydrogen PeroxideNitric OxideRNATelomerasetelomerase RNATert protein, mouseangiotensin IIflow-mediated dilationmicrocirculationtelomerasetelomerase reverse transcriptase

Identifiers

PMID29351466
PMCPMC6008150
OpenAlexW2778000367

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.