Evidence map›Paper›PMID 37863894›Full record

ReviewCell death & disease2023

Macrophage polarization and metabolism in atherosclerosis.

Pengbo Hou, Jiankai Fang, Zhanhong Liu, Yufang Shi, Massimiliano Agostini, Francesca Bernassola, Pierluigi Bove, Eleonora Candi, Valentina Rovella, Giuseppe Sica and 6 more

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 1 pooled it
44.4field-weighted citation impact, top 1% 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

209 citing papers in PubMed, 1 synthesis or guideline pooled it, 270 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Ilexoside K Ameliorates Atherosclerosis by Suppressing CD72Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  10. The role of type I collagen in white matter injury.Anatomical science international · 2026
    Review
  11. Furong Tongmai Capsule Ameliorates Atherosclerosis in ApoEJournal of cellular and molecular medicine · 2026
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

149 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

16 authors at 2 institutions in 2 countries.

Pengbo HouDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Jiankai FangThe First Affiliated Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Suzhou Medical College of Soochow University, Suzhou, China.
Zhanhong LiuDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Yufang ShiThe First Affiliated Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Suzhou Medical College of Soochow University, Suzhou, China.
Massimiliano AgostiniDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.ORCID 0000-0003-3124-2072
Francesca BernassolaDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Pierluigi BoveDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Eleonora CandiDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.ORCID 0000-0001-8332-4825
Valentina RovellaDepartment of System Medicine, University of Rome Tor Vergata, Rome, Italy.
Giuseppe SicaDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Qiang SunDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.ORCID 0000-0002-5342-0637
Ying WangDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.ORCID 0000-0002-2571-9367
Manuel ScimecaDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy.
Massimo FedericiDepartment of System Medicine, University of Rome Tor Vergata, Rome, Italy. federicm@uniroma2.it.ORCID 0000-0003-4989-5194
Alessandro MaurielloDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy. alessandro.mauriello@uniroma2.it.ORCID 0000-0002-7351-5676
Gerry MelinoDepartment of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy. melino@uniroma2.it.ORCID 0000-0001-9428-5972
University of Rome Tor Vergata · ITSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of fatty deposits in the inner walls of vessels. These plaques restrict blood flow and lead to complications such as heart attack or stroke. The development of atherosclerosis is influenced by a variety of factors, including age, genetics, lifestyle, and underlying health conditions such as high blood pressure or diabetes. Atherosclerotic plaques in stable form are characterized by slow growth, which leads to luminal stenosis, with low embolic potential or in unstable form, which contributes to high risk for thrombotic and embolic complications with rapid clinical onset. In this complex scenario of atherosclerosis, macrophages participate in the whole process, including the initiation, growth and eventually rupture and wound healing stages of artery plaque formation. Macrophages in plaques exhibit high heterogeneity and plasticity, which affect the evolving plaque microenvironment, e.g., leading to excessive lipid accumulation, cytokine hyperactivation, hypoxia, apoptosis and necroptosis. The metabolic and functional transitions of plaque macrophages in response to plaque microenvironmental factors not only influence ongoing and imminent inflammatory responses within the lesions but also directly dictate atherosclerotic progression or regression. In this review, we discuss the origin of macrophages within plaques, their phenotypic diversity, metabolic shifts, and fate and the roles they play in the dynamic progression of atherosclerosis. It also describes how macrophages interact with other plaque cells, particularly T cells. Ultimately, targeting pathways involved in macrophage polarization may lead to innovative and promising approaches for precision medicine. Further insights into the landscape and biological features of macrophages within atherosclerotic plaques may offer valuable information for optimizing future clinical treatment for atherosclerosis by targeting macrophages.

Indexed as

AtherosclerosisMyocardial InfarctionPlaque, AtheroscleroticApoptosisHumansMacrophages

Identifiers

PMID37863894
PMCPMC10589261
OpenAlexW4387806924

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.