Evidence map›Paper›PMID 34122329›Full record

ArticleFrontiers in endocrinology2021

Crosstalk Between LXR and Caveolin-1 Signaling Supports Cholesterol Efflux and Anti-Inflammatory Pathways in Macrophages.

Cristina M Ramírez, Marta Torrecilla-Parra, Virginia Pardo-Marqués, Mario Fernández de-Frutos, Ana Pérez-García, Carlos Tabraue, Juan Vladimir de la Rosa, Patricia Martín-Rodriguez, Mercedes Díaz-Sarmiento, Uxue Nuñez and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Reprogramming of the LXRα Transcriptome Sustains Macrophage Secondary Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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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

15 authors at 5 institutions in 1 country.

Cristina M RamírezInstituto Madrileño de Estudios Avanzados (IMDEA) Research Institute of Food and Health Sciences, Madrid, Spain.
Marta Torrecilla-ParraInstituto Madrileño de Estudios Avanzados (IMDEA) Research Institute of Food and Health Sciences, Madrid, Spain.
Virginia Pardo-MarquésInstituto Madrileño de Estudios Avanzados (IMDEA) Research Institute of Food and Health Sciences, Madrid, Spain.
Mario Fernández de-FrutosInstituto Madrileño de Estudios Avanzados (IMDEA) Research Institute of Food and Health Sciences, Madrid, Spain.
Ana Pérez-GarcíaInstituto Madrileño de Estudios Avanzados (IMDEA) Research Institute of Food and Health Sciences, Madrid, Spain.
Carlos TabraueUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Juan Vladimir de la RosaUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Patricia Martín-RodriguezUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Mercedes Díaz-SarmientoUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Uxue NuñezUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Marta C OrizaolaInstituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas CSIC-Universidad Autónoma de Madrid, Madrid, Spain.
Paqui G TravésInstituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas CSIC-Universidad Autónoma de Madrid, Madrid, Spain.
Marta CampsInstitut de Biomedicina (IBUB), Universitat de Barcelona, Barcelona, Spain.
Lisardo BoscáUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Antonio CastrilloUnidad de Biomedicina (Unidad Asociada al CSIC), Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS) de la Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
Madrid Institute for Advanced Studies · ESUniversidad de Las Palmas de Gran Canaria · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Investigaciones Biomédicas Sols-Morreale · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are immune cells that play crucial roles in host defense against pathogens by triggering their exceptional phagocytic and inflammatory functions. Macrophages that reside in healthy tissues also accomplish important tasks to preserve organ homeostasis, including lipid uptake/efflux or apoptotic-cell clearance. Both homeostatic and inflammatory functions of macrophages require the precise stability of lipid-rich microdomains located at the cell membrane for the initiation of downstream signaling cascades. Caveolin-1 (Cav-1) is the main protein responsible for the biogenesis of caveolae and plays an important role in vascular inflammation and atherosclerosis. The Liver X receptors (LXRs) are key transcription factors for cholesterol efflux and inflammatory gene responses in macrophages. Although the role of Cav-1 in cellular cholesterol homeostasis and vascular inflammation has been reported, the connection between LXR transcriptional activity and Cav-1 expression and function in macrophages has not been investigated. Here, using gain and loss of function approaches, we demonstrate that LXR-dependent transcriptional pathways modulate Cav-1 expression and compartmentation within the membrane during macrophage activation. As a result, Cav-1 participates in LXR-dependent cholesterol efflux and the control of inflammatory responses. Together, our data show modulation of the LXR-Cav-1 axis could be exploited to control exacerbated inflammation and cholesterol overload in the macrophage during the pathogenesis of lipid and immune disorders, such as atherosclerosis.

Indexed as

AnimalsAnti-Inflammatory AgentsApolipoprotein A-IAtherosclerosisATP Binding Cassette Transporter 1Caveolin 1Cell MembraneCholesterolDetergentsGene ExpressionGreen Fluorescent ProteinsHumansInflammationLiver X ReceptorsMacrophagesMiceAbca1 protein, mouseAnti-Inflammatory AgentsAPOA1 protein, humanApolipoprotein A-IATP Binding Cassette Transporter 1Cav1 protein, mouseCaveolin 1CholesterolDetergentsGreen Fluorescent ProteinsLiver X Receptorscaveolin-1cholesterol effluxgene expressioninflammationLXRmacrophage

Identifiers

PMID34122329
PMCPMC8190384
OpenAlexW3172307058

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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.