Evidence map›Paper›PMID 40130825›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2025

IL-6 induces mitochondrial ROS production and blunts NO bioavailability in human aortic endothelial cells.

Prema Velusamy, David J Buckley, Jody L Greaney, Adam J Case, Paul J Fadel, Daniel W Trott

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

6 authors.

Prema VelusamyDepartment of Kinesiology, University of Texas at Arlington, Arlington, Texas, United States.ORCID 0000-0002-9843-1364
David J BuckleyDepartment of Kinesiology, University of Texas at Arlington, Arlington, Texas, United States.ORCID 0000-0002-0145-8764
Jody L GreaneyDepartment of Health Behavior and Nutrition Sciences, University of Delaware, Newark, Delaware, United States.ORCID 0000-0002-9855-3978
Adam J CaseDepartment of Psychiatry and Behavioral Sciences, Texas A&M University, College Station, Texas, United States.ORCID 0000-0003-3404-1428
Paul J FadelDepartment of Kinesiology, University of Texas at Arlington, Arlington, Texas, United States.ORCID 0000-0002-0115-0743
Daniel W TrottDepartment of Kinesiology, University of Texas at Arlington, Arlington, Texas, United States.ORCID 0000-0003-4872-4422

Funding

IMPACT OF T CELLS ON AGE-RELATED VASCULAR DYSFUNCTION: A TRANSLATIONAL APPROACH - DIVERSITY SUPPLEMENTR01AG060395 · NIA · UNIVERSITY OF UTAH · PI DONATO, ANTHONY JOHN · 2019 to 2023
$2.5M
Mechanisms of CD8+ mediated cell non-autonomous arterial agingR01AG086447 · NIA · UNIVERSITY OF TEXAS ARLINGTON · PI Daniel Trott · 2024 to 2026
$1.8M
T cells mediate age related arterial dysfunctionK01AG061271 · NIA · UNIVERSITY OF TEXAS ARLINGTON · PI TROTT, DANIEL · 2019 to 2023
$635k
Daily stress processes and sympathetic reactivity in depressionR21MH123928 · NIMH · UNIVERSITY OF TEXAS ARLINGTON · PI GREANEY, JODY · 2021 to 2022
$521k
American Heart Association (AHA) AHA940023HHS | NIH | National Institute of Mental Health (NIMH) MH123928HHS | NIH | National Institute on Aging (NIA) K01AG061271HHS | NIH | National Institute on Aging (NIA) R01AG060395HHS | NIH | National Institute on Aging (NIA) R01AG086447Moritz Chair in GeriatricsNIA NIH HHS K01 AG061271NIA NIH HHS R01 AG060395NIA NIH HHS R01 AG086447NIMH NIH HHS R21 MH123928
6 · The paper itself

Abstract

Chronic inflammation is a major contributor to the development of endothelial dysfunction. Circulating concentrations of the proinflammatory cytokine interleukin-6 (IL-6) have been shown to predict cardiovascular disease risk and are associated with the development of vascular dysfunction. However, the mechanisms that underlie inflammation-induced endothelial dysfunction are not fully understood. Vascular endothelial dysfunction is characterized by blunted nitric oxide (NO) bioavailability and increased reactive oxygen species (ROS), with mitochondrial ROS suggested to play a primary role. Therefore, we tested the hypothesis that IL-6 induces mitochondrial ROS production and blunts NO bioavailability in endothelial cells. To study the effect of IL-6, we treated the human aortic endothelial cells (HAECs) with IL-6, MitoTEMPOL (MT; a mitochondria-targeted antioxidant), and/or a nitric oxide synthase (NOS) inhibitor (l-NAME) with and without ACh stimulation. Results are expressed as means ± SD (

Indexed as

AortaEndothelial CellsInterleukin-6MitochondriaNitric OxideReactive Oxygen SpeciesBiological AvailabilityCells, CulturedHumansIL6 protein, humanInterleukin-6Nitric OxideReactive Oxygen SpeciesendotheliuminflammationMitoTEMPOLvascular dysfunction

Identifiers

PMID40130825
PMCPMC12232744

What OpenQuestion holds

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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.