Evidence map›Paper›PMID 38136180›Full record

ArticleAntioxidants (Basel, Switzerland)2023

Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension.

Simin Yan, Joshua R Sheak, Benjimen R Walker, Nikki L Jernigan, Thomas C Resta

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  17. Mitochondrial Dysfunction in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023
    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.

Simin YanVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Joshua R SheakVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.ORCID 0000-0002-8002-4365
Benjimen R WalkerVascular 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.ORCID 0000-0001-6269-2274
Thomas C RestaVascular 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

MINORITY INSTITUTIONAL RESEARCH TRAINING PROGRAM (T32)T32HL007736 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 1993 to 2025
$6.5M
Vascular Smooth Muscle Function in Pulmonary HypertensionR01HL111084 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI JERNIGAN, NIKKI L · 2013 to 2022
$3.4M
Oxidant Signaling in Pulmonary HypertensionR01HL169945 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI THOMAS C RESTA · 2023 to 2026
$2.3M
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
Role of PKCbeta and oxidant signaling in neonatal pulmonary hypertensionF31HL131334 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI SHEAK, JOSHUA ROGER · 2016 to 2017
$47k
NHLBI NIH HHS F31 HL131334NHLBI NIH HHS R01 HL111084NHLBI NIH HHS R01 HL132883NHLBI NIH HHS R01 HL169945NHLBI NIH HHS T32 HL007736
6 · The paper itself

Abstract

Pulmonary hypertension (PH) resulting from chronic hypoxia (CH) occurs in patients with chronic obstructive pulmonary diseases, sleep apnea, and restrictive lung diseases, as well as in residents at high altitude. Previous studies from our group and others demonstrate a detrimental role of reactive oxygen species (ROS) in the pathogenesis of CH-induced PH, although the subcellular sources of ROS are not fully understood. We hypothesized that mitochondria-derived ROS (mtROS) contribute to enhanced vasoconstrictor reactivity and PH following CH. To test the hypothesis, we exposed rats to 4 weeks of hypobaric hypoxia (P

Indexed as

hypoxiamitochondriapulmonary hypertensionreactive oxygen speciesvasoconstriction

Identifiers

PMID38136180
PMCPMC10741244
OpenAlexW4389187901

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.