Evidence map›Paper›PMID 35387480›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2022

2021 Jeffrey M. Hoeg Award Lecture: Defining the Role of Efferocytosis in Cardiovascular Disease: A Focus on the CD47 (Cluster of Differentiation 47) Axis.

Kai-Uwe Jarr, Yoko Kojima, Irving L Weissman, Nicholas J Leeper

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Efferocytosis in atherosclerosis.Nature reviews. Cardiology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Role of vascular smooth muscle cell clonality in atherosclerosis.Frontiers in cardiovascular medicine · 2023
    Review
  13. Article
  14. The Role of Hydrogen Sulfide in Plaque Stability.Antioxidants (Basel, Switzerland) · 2022
    Review
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 3 institutions in 2 countries.

Kai-Uwe JarrDepartment of Surgery, Division of Vascular Surgery, Stanford University School of Medicine, CA (K.-U.J., Y.K., N.J.L.).ORCID 0000-0003-3376-6478
Yoko KojimaDepartment of Surgery, Division of Vascular Surgery, Stanford University School of Medicine, CA (K.-U.J., Y.K., N.J.L.).
Irving L WeissmanStanford Institute for Stem Cell Biology and Regenerative Medicine (I.L.W.), Stanford University, CA.
Nicholas J LeeperDepartment of Surgery, Division of Vascular Surgery, Stanford University School of Medicine, CA (K.-U.J., Y.K., N.J.L.).ORCID 0000-0002-0905-2806
Stanford University · USCalifornia Institute for Regenerative Medicine · USCardiovascular Institute of the South · US

Funding

Clonal expansion, resistance to efferocytosis and innate immunity in atherosclerosisR35HL144475 · NHLBI · STANFORD UNIVERSITY · PI LEEPER, NICHOLAS JAMES · 2019 to 2024
$5.1M
NHLBI NIH HHS R35 HL144475
6 · The paper itself

Abstract

A key feature of atherogenesis is the accumulation of diseased and dying cells within the lesional necrotic core. While the burden of intraplaque apoptotic cells may be driven in part by an increase in programmed cell death, mounting evidence suggests that their presence may primarily be dictated by a defect in programmed cell removal, or efferocytosis. In this brief review, we will summarize the evidence suggesting that inflammation-dependent changes within the plaque render target cells inedible and reduce the appetite of lesional phagocytes. We will present the genetic causation studies, which indicate these phenomena promote lesion expansion and plaque vulnerability, and the interventional data which suggest that these processes can be reversed. Particular emphasis is provided related to the antiphagocytic CD47 (cluster of differentiation 47) do not eat me axis, which has emerged as a novel antiatherosclerotic translational target that is predicted to provide benefit independent of traditional cardiovascular risk factors.

Indexed as

Awards and PrizesCardiovascular DiseasesPlaque, AtheroscleroticApoptosisCD47 AntigenHumansMacrophagesPhagocytosisCD47 AntigenCD47 protein, humanatherosclerosiscardiovascular diseasesefferocytosisinflammationrisk factors

Identifiers

PMID35387480
PMCPMC9183217
OpenAlexW4224298042

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.