Evidence map›Paper›PMID 29997514›Full record

ReviewFrontiers in physiology2018

Lipid and Non-lipid Factors Affecting Macrophage Dysfunction and Inflammation in Atherosclerosis.

Mark S Gibson, Neuza Domingues, Otilia V Vieira

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Review
  3. The Emerging Role of Senolysis in Atherosclerosis.Medicina (Kaunas, Lithuania) · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Frontiers in immunology · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. bioRxiv : the preprint server for biology · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Mark S GibsonLysosomes in Chronic Human Pathologies and Infection, Faculdade de Ciências Médicas, Centro de Estudos de Doenças Crónicas, NOVA Medical School, Universidade NOVA de Lisboa, Lisbon, Portugal.
Neuza DominguesLysosomes in Chronic Human Pathologies and Infection, Faculdade de Ciências Médicas, Centro de Estudos de Doenças Crónicas, NOVA Medical School, Universidade NOVA de Lisboa, Lisbon, Portugal.
Otilia V VieiraLysosomes in Chronic Human Pathologies and Infection, Faculdade de Ciências Médicas, Centro de Estudos de Doenças Crónicas, NOVA Medical School, Universidade NOVA de Lisboa, Lisbon, Portugal.
Universidade Nova de Lisboa · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease and a leading cause of human mortality. The lesional microenvironment contains a complex accumulation of variably oxidized lipids and cytokines. Infiltrating monocytes become polarized in response to these stimuli, resulting in a broad spectrum of macrophage phenotypes. The extent of lipid loading in macrophages influences their phenotype and consequently their inflammatory status. In response to excess atherogenic ligands, many normal cell processes become aberrant following a loss of homeostasis. This can have a direct impact upon the inflammatory response, and conversely inflammation can lead to cell dysfunction. Clear evidence for this exists in the lysosomes, endoplasmic reticulum and mitochondria of atherosclerotic macrophages, the principal lesional cell type. Furthermore, several intrinsic cell processes become dysregulated under lipidotic conditions. Therapeutic strategies aimed at restoring cell function under disease conditions are an ongoing coveted aim. Macrophages play a central role in promoting lesional inflammation, with plaque progression and stability being directly proportional to macrophage abundance. Understanding how mixtures or individual lipid species regulate macrophage biology is therefore a major area of atherosclerosis research. In this review, we will discuss how the myriad of lipid and lipoprotein classes and products used to model atherogenic, proinflammatory immune responses has facilitated a greater understanding of some of the intricacies of chronic inflammation and cell function. Despite this, lipid oxidation produces a complex mixture of products and with no single or standard method of derivatization, there exists some variation in the reported effects of certain oxidized lipids. Likewise, differences in the methods used to generate macrophages

Indexed as

atherosclerosischronic inflammationlysosome dysfunctionmacrophage heterogeneityoxidized lipids

Identifiers

PMID29997514
PMCPMC6029489
OpenAlexW2810856837

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.