Evidence map›Paper›PMID 37595492›Full record

ReviewInternational immunopharmacology2023

Etiology of lipid-laden macrophages in the lung.

E R Stevenson, L C Smith, M L Wilkinson, S J Lee, A J Gow

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

E R StevensonDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, United States.
L C SmithDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, United States; Department of Pharmaceutical Sciences, University of Connecticut School of Pharmacy, Storrs, CT, United States.
M L WilkinsonDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, United States.
S J LeeDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, United States.
A J GowDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, United States.
Rutgers, The State University of New Jersey · US

Funding

Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI BRIAN T BUCKLEY · 1988 to 2026
$47.4M
TRAINING IN EVIRONMENTAL TOXICOLOGYT32ES007148 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Lauren M Aleksunes · 1987 to 2026
$11.4M
NO-Modified Biomolecules and Pulmonary SignalingR01HL086621 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI GOW, ANDREW J · 2008 to 2016
$2.8M
Obstructive Sleep Apnea and WTC dust: Does Chronic Intermittent Hypoxia exacerbate WTC dust induced lung injuryU01OH012072 · OH · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI GOW, ANDREW J, SUNDERRAM, JAG · 2021 to 2022
$1.0M
Estrogen receptor signaling, inflammation and ozone toxicityR00ES032473 · NIEHS · UNIVERSITY OF CONNECTICUT STORRS · PI SMITH, LEY C · 2023 to 2025
$745k
Estrogen receptor signaling, inflammation and ozone toxicityK99ES032473 · NIEHS · RUTGERS, THE STATE UNIV OF N.J. · PI SMITH, LEY C · 2021 to 2022
$236k
Ozone toxicity: targeting the resolution of inflammationF32ES030984 · NIEHS · RUTGERS, THE STATE UNIV OF N.J. · PI SMITH, LEY C · 2019 to 2019
$64k
NHLBI NIH HHS R01 HL086621NIEHS NIH HHS F32 ES030984NIEHS NIH HHS K99 ES032473NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R00 ES032473NIEHS NIH HHS T32 ES007148NIOSH CDC HHS U01 OH012072
6 · The paper itself

Abstract

Uniquely positioned as sentinel cells constantly exposed to the environment, pulmonary macrophages are vital for the maintenance of the lung lining. These cells are responsible for the clearance of xenobiotics, pathogen detection and clearance, and homeostatic functions such as surfactant recycling. Among the spectrum of phenotypes that may be expressed by macrophages in the lung, the pulmonary lipid-laden phenotype is less commonly studied in comparison to its circulatory counterpart, the atherosclerotic lesion-associated foam cell, or the acutely activated inflammatory macrophage. Herein, we propose that lipid-laden macrophage formation in the lung is governed by lipid acquisition, storage, metabolism, and export processes. The cellular balance of these four processes is critical to the maintenance of homeostasis and the prevention of aberrant signaling that may contribute to lung pathologies. This review aims to examine mechanisms and signaling pathways that are involved in lipid-laden macrophage formation and the potential consequences of this phenotype in the lung.

Indexed as

MacrophagesMacrophages, AlveolarFoam CellsLipidsLungLipidsFoam cellImmunometabolismInflammationLipidLungMacrophage

Identifiers

PMID37595492
PMCPMC10734282
OpenAlexW4385861005

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.