Evidence map›Paper›PMID 41047668›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2025

Shear Stress Regulates ABCA1-Dependent Membrane Cholesterol Content in Endothelial Cells Facilitating H

Jacob R Anderson, Nancy L Kanagy, Laura V Gonzalez Bosc, Jay S Naik

Abstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Jacob R AndersonDepartment of Cell Biology and Physiology, University of New Mexico Health Science Center, MSC08 4750, Albuquerque, New Mexico, USA.
Nancy L KanagyDepartment of Cell Biology and Physiology, University of New Mexico Health Science Center, MSC08 4750, Albuquerque, New Mexico, USA.
Laura V Gonzalez BoscDepartment of Cell Biology and Physiology, University of New Mexico Health Science Center, MSC08 4750, Albuquerque, New Mexico, USA.
Jay S NaikDepartment of Cell Biology and Physiology, University of New Mexico Health Science Center, MSC08 4750, Albuquerque, New Mexico, USA.

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
MINORITY INSTITUTIONAL RESEARCH TRAINING PROGRAM (T32)T32HL007736 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 1993 to 2025
$6.5M
Regulation of H2S signaling in vascular functionR01HL160606 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI NAIK, JAY S · 2022 to 2025
$2.1M
NCI NIH HHS P30 CA118100NHLBI NIH HHS R01 HL160606NHLBI NIH HHS T32 HL007736NIH HHS 5T32HL007736-25NIH HHS HL160606-01NIH HHS P30CA118100
6 · The paper itself

Abstract

Endothelial cells (ECs) express an array of integral membrane proteins, including ion channels and transporters that contribute to blood flow regulation and cell-cell communication. Many of these membrane proteins are regulated by plasma membrane cholesterol content. The ATP-binding cassette family A1 (ABCA1) transporter is a regulator of membrane cholesterol content. We have shown increased ABCA1 mRNA expression and reduced EC membrane cholesterol in resistance mesenteric arteries compared to conduit arteries. Previous studies suggest shear stress (SS) can increase or decrease ABCA1 expression in a cell-type-dependent manner. HYPOTHESIS: SS sustains lower EC membrane cholesterol concentration through ABCA1-mediated cholesterol transport, facilitating H

methodsThe effect of SS on ABCA1 and membrane cholesterol content was assessed in pressurized mesenteric arteries from male Sprague-Dawley rats and cultured human aortic endothelial cells. Pressure myography was used to assess the effects of ABCA1 inhibition on H

resultsSS increased ABCA1 expression in the endothelium of mesenteric arteries and cultured human aortic endothelial cells and markedly reduced EC membrane cholesterol. Inhibition of ABCA1 increased EC membrane cholesterol content and abolished H

conclusionSS facilitation of EC-dependent vasodilation appears to be mediated by membrane cholesterol content.

Indexed as

ATP Binding Cassette Transporter 1Cell MembraneCholesterolEndothelial CellsHydrogen SulfideStress, MechanicalVasodilationAnimalsCells, CulturedHumansMaleMesenteric ArteriesRatsRats, Sprague-DawleyABCA1 protein, humanAbca1 protein, ratATP Binding Cassette Transporter 1CholesterolHydrogen Sulfidehydrogen sulfidemesentericshear stressSprague–Dawley ratvasodilation

Identifiers

PMID41047668
PMCPMC12498007

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Registered trials

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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.