Evidence map›Paper›PMID 28674080›Full record

ArticleEMBO molecular medicine2017

Macrophage deficiency of miR-21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis.

Alberto Canfrán-Duque, Noemi Rotllan, Xinbo Zhang, Marta Fernández-Fuertes, Cristina Ramírez-Hidalgo, Elisa Araldi, Lidia Daimiel, Rebeca Busto, Carlos Fernández-Hernando, Yajaira Suárez

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Research progress on macrophage regulation of atherosclerosis.Frontiers in cardiovascular medicine · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025
    Review
  17. Review
  18. Review
  19. Article
  20. Review

57 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

10 authors at 2 institutions in 2 countries.

Alberto Canfrán-DuqueVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Noemi RotllanVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Xinbo ZhangVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Marta Fernández-FuertesVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Cristina Ramírez-HidalgoVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Elisa AraldiVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Lidia DaimielVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA.
Rebeca BustoServicio de Bioquímica-Investigación, Hospital Universitario Ramón y Cajal de Investigación Sanitaria (IRyCIS), Madrid, Spain.
Carlos Fernández-HernandoVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA carlos.fernandez@yale.edu yajaira.suarez@yale.edu.ORCID 0000-0002-3950-1924
Yajaira SuárezVascular Biology and Therapeutics Program, Integrative Cell Signaling and Neurobiology of Metabolism Program and the Departments of Comparative Medicine and Pathology, Yale University School of Medicine, New Haven, CT, USA carlos.fernandez@yale.edu yajaira.suarez@yale.edu.ORCID 0000-0003-4549-2953
Yale University · USCentro de Investigación Biomédica en Red · ES

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold, GERALD I SHULMAN · 1993 to 2026
$44.0M
microRNAs in vascular diseasesR01HL105945 · NHLBI · YALE UNIVERSITY · PI SUAREZ, YAJAIRA · 2011 to 2020
$3.7M
Caveolin-1 in Lipoprotein Metabolism and Atherosclerosis.R01HL106063 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.5M
Role of microRNAs in lipid metabolism and cardiovascular diseaseR01HL107953 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.4M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL105945NHLBI NIH HHS R01 HL106063NHLBI NIH HHS R01 HL107953NIDDK NIH HHS P30 DK045735
6 · The paper itself

Abstract

Atherosclerosis, the major cause of cardiovascular disease, is a chronic inflammatory disease characterized by the accumulation of lipids and inflammatory cells in the artery wall. Aberrant expression of microRNAs has been implicated in the pathophysiological processes underlying the progression of atherosclerosis. Here, we define the contribution of miR-21 in hematopoietic cells during atherogenesis. Interestingly, we found that miR-21 is the most abundant miRNA in macrophages and its absence results in accelerated atherosclerosis, plaque necrosis, and vascular inflammation. miR-21 expression influences foam cell formation, sensitivity to ER-stress-induced apoptosis, and phagocytic clearance capacity. Mechanistically, we discovered that the absence of miR-21 in macrophages increases the expression of the miR-21 target gene, MKK3, promoting the induction of p38-CHOP and JNK signaling. Both pathways enhance macrophage apoptosis and promote the post-translational degradation of ABCG1, a transporter that regulates cholesterol efflux in macrophages. Altogether, these findings reveal a major role for hematopoietic miR-21 in atherogenesis.

Indexed as

ApoptosisAnimalsAtherosclerosisATP Binding Cassette Transporter, Subfamily G, Member 1Blood VesselsFemaleHumansMacrophagesMaleMAP Kinase Kinase 3Mice, Inbred C57BLMice, KnockoutMicroRNAsNecrosisATP Binding Cassette Transporter, Subfamily G, Member 1MAP Kinase Kinase 3MicroRNAsMIRN21 microRNA, mouseapoptosisatherosclerosismacrophage polarizationmiRNA

Identifiers

PMID28674080
PMCPMC5582411
OpenAlexW2731656009

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.