Evidence map›Paper›PMID 32394286›Full record

ArticleInflammation2020

Electronegative LDL Induces M1 Polarization of Human Macrophages Through a LOX-1-Dependent Pathway.

Shwu-Fen Chang, Po-Yuan Chang, Yuan-Chun Chou, Shao-Chun Lu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. 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
1.1field-weighted citation impact, top 24% 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, 23 citations in OpenAlex.

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  6. Can Electronegative LDL Act as a Multienzymatic Complex?International journal of molecular sciences · 2023
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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

4 authors at 2 institutions in 1 country.

Shwu-Fen ChangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Po-Yuan ChangDepartment of Internal Medicine, Cardiovascular Center and Division of Cardiology, College of Medicine, National Taiwan university, Taipei, Taiwan.
Yuan-Chun ChouDepartment of Biochemistry and Molecular Biology; College of Medicine, National Taiwan university, No. 1, Jen Ai Road Section 1, Taipei, 100233, Taiwan.
Shao-Chun LuDepartment of Biochemistry and Molecular Biology; College of Medicine, National Taiwan university, No. 1, Jen Ai Road Section 1, Taipei, 100233, Taiwan. lsc@ntu.edu.tw.
National Taiwan University · TWTaipei Medical University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 105-2320-B-002-030-MY3
6 · The paper itself

Abstract

In response to environmental stimuli, monocytes undergo polarization into classically activated (M1) or alternatively activated (M2) states. M1 and M2 macrophages exert opposing pro- and anti-inflammatory properties, respectively. Electronegative low-density lipoprotein (LDL) (LDL(-)) is a naturally occurring mildly oxidized LDL found in the plasma of patients with hypercholesterolemia, diabetes, and acute myocardial infarction, and has been shown to involve in the pathogenesis of atherosclerosis. In this study, we examined the effects of LDL(-) on macrophage polarization and the involvement of lectin-like oxidized LDL receptor-1 (LOX-1) in this process. THP-1 macrophages were treated with native LDL (nLDL) or LDL(-), and then the expression of M1/M2-related surface markers and cytokines were evaluated. The results show that treatment with LDL(-) resulted in profound increase in proinflammatory cytokines, IL-1β, IL-6, and TNF-α, and M1-surface marker CD86; however, M2-related cytokines, IL-10 and TGF-β, and M2-surface marker CD206 were not changed by LDL(-). Untreated or nLDL-treated cells were used as control. LDL(-)-induced M1 polarization and secretion of proinflammatory cytokines were diminished in LOX-1 knockdown cells. Taken together, the results show that LDL(-) promotes differentiation of human monocytes to M1 macrophages through a LOX-1-dependent pathway, and explore the contribution of LDL(-) and LOX-1 to the development of chronic inflammation in atherosclerosis.

Indexed as

AnimalsCell PolarityDiet, High-FatHumansLipoproteins, LDLMacrophagesMaleRabbitsScavenger Receptors, Class ESignal TransductionTHP-1 CellsLipoproteins, LDLOLR1 protein, humanoxidized low density lipoproteinScavenger Receptors, Class EElectronegative LDLLOX-1Macrophage polarization

Identifiers

PMID32394286
OpenAlexW3024146050

What OpenQuestion holds

Textmetadata
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.