Evidence map›Paper›PMID 33076504›Full record

ReviewAntioxidants (Basel, Switzerland)2020

Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.

Simin Yan, Thomas C Resta, Nikki L Jernigan

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Smooth muscle Rac1 contributes to pulmonary hypertension.British journal of pharmacology · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Simin YanVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Thomas C RestaVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Nikki L JerniganVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
University of New Mexico · US

Funding

Vascular Smooth Muscle Function in Pulmonary HypertensionR01HL111084 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI JERNIGAN, NIKKI L · 2013 to 2022
$3.4M
Pulmonary Vasoreactivity Following Chronic HypoxiaR01HL088192 · NHLBI · UNIVERSITY OF NEW MEXICO · PI RESTA, THOMAS C · 2008 to 2012
$1.9M
Vascular Smooth Muscle Signaling in Intermittent Hypoxia-Induced Pulmonary HypertensionR01HL132883 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 2016 to 2019
$1.5M
NHLBI NIH HHS R01 HL088192NHLBI NIH HHS R01 HL111084NHLBI NIH HHS R01 HL132883NIH HHS R01 HL 132883 to T.C.R. and R01 HL 111084 to N.L.J.
6 · The paper itself

Abstract

Elevated resistance of pulmonary circulation after chronic hypoxia exposure leads to pulmonary hypertension. Contributing to this pathological process is enhanced pulmonary vasoconstriction through both calcium-dependent and calcium sensitization mechanisms. Reactive oxygen species (ROS), as a result of increased enzymatic production and/or decreased scavenging, participate in augmentation of pulmonary arterial constriction by potentiating calcium influx as well as activation of myofilament sensitization, therefore mediating the development of pulmonary hypertension. Here, we review the effects of chronic hypoxia on sources of ROS within the pulmonary vasculature including NADPH oxidases, mitochondria, uncoupled endothelial nitric oxide synthase, xanthine oxidase, monoamine oxidases and dysfunctional superoxide dismutases. We also summarize the ROS-induced functional alterations of various Ca

Indexed as

calcium influxcalcium sensitizationchronic hypoxiapulmonary hypertensionpulmonary vasoconstrictionreactive oxygen species

Identifiers

PMID33076504
PMCPMC7602539
OpenAlexW3093069358

What Socratic 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 Socratic graph.