Evidence map›Paper›PMID 33380171›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2021

Trained Immunity and Reactivity of Macrophages and Endothelial Cells.

Charles Drummer, Fatma Saaoud, Ying Shao (邵颖), Yu Sun (孙宇), Keman Xu (徐克曼), Yifan Lu (路一凡), Dong Ni (倪栋), Diana Atar, Xiaohua Jiang (蒋晓华), Hong Wang (王虹) and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
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  11. Assessment ofOpen veterinary journal · 2026
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  13. Review
  14. Review
  15. Review
  16. Article
  17. Trained immunity in lung injury and repair.Frontiers in immunology · 2026
    Review
  18. Article
  19. Article
  20. Review

18 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Charles Drummer *Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Fatma Saaoud *Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Ying Shao (邵颖)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Yu Sun (孙宇)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Keman Xu (徐克曼)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Yifan Lu (路一凡)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Dong Ni (倪栋)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Diana AtarCardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Xiaohua Jiang (蒋晓华)Cardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Hong Wang (王虹)Metabolic Disease Research (X.J., H.W., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Xiaofeng YangCardiovascular Research Center, Centers for Inflammation, Translational and Clinical Lung Research and Thrombosis Research (C.D., F.S., Y. Shao, Y. Sun, K.X., Y.L., D.N., D.A., X.J., X.Y.), Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Temple University · US

Funding

CD40 monocyte in chronic kidney diseaseR01DK113775 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2017 to 2021
$3.3M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
The roles of miR-155 in regulating atherosclerosis and metabolically healthy obesityR01HL138749 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.6M
IL-35 inhibits gut microbiota-produced uremic toxin-accelerated endothelial cell activationR01HL147565 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2019 to 2022
$2.6M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL138749NHLBI NIH HHS R01 HL147565NIDDK NIH HHS R01 DK104116NIDDK NIH HHS R01 DK113775
6 · The paper itself

Abstract

Innate immune cells can develop exacerbated immunologic response and long-term inflammatory phenotype following brief exposure to endogenous or exogenous insults, which leads to an altered response towards a second challenge after the return to a nonactivated state. This phenomenon is known as trained immunity (TI). TI is not only important for host defense and vaccine response but also for chronic inflammations such as cardiovascular and metabolic diseases such as atherosclerosis. TI can occur in innate immune cells such as monocytes/macrophages, natural killer cells, endothelial cells (ECs), and nonimmune cells, such as fibroblast. In this brief review, we analyze the significance of TI in ECs, which are also considered as innate immune cells in addition to macrophages. TI can be induced by a variety of stimuli, including lipopolysaccharides, BCG (bacillus Calmette-Guerin), and oxLDL (oxidized low-density lipoprotein), which are defined as risk factors for cardiovascular and metabolic diseases. Furthermore, TI in ECs is functional for inflammation effectiveness and transition to chronic inflammation. Rewiring of cellular metabolism of the trained cells takes place during induction of TI, including increased glycolysis, glutaminolysis, increased accumulation of tricarboxylic acid cycle metabolites and acetyl-coenzyme A production, as well as increased mevalonate synthesis. Subsequently, this leads to epigenetic remodeling, resulting in important changes in chromatin architecture that enables increased gene transcription and enhanced proinflammatory immune response. However, TI pathways and inflammatory pathways are separated to ensure memory stays when inflammation undergoes resolution. Additionally, reactive oxygen species play context-dependent roles in TI. Therefore, TI plays significant roles in EC and macrophage pathology and chronic inflammation. However, further characterization of TI in ECs and macrophages would provide novel insights into cardiovascular disease pathogenesis and new therapeutic targets. Graphic Abstract: A graphic abstract is available for this article.

Indexed as

AnimalsCardiovascular DiseasesCytokinesEndothelial CellsEnergy MetabolismEpigenesis, GeneticHumansImmunity, InnateImmunologic MemoryInfectionsInflammationMacrophagesMetabolic DiseasesMetabolic Networks and PathwaysModels, ImmunologicalReactive Oxygen SpeciesCytokinesReactive Oxygen Speciesatherosclerosiscardiovascular diseasesendothelial cellsmacrophagestrained immunity

Identifiers

PMID33380171
PMCPMC7904591
OpenAlexW3116478764

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.