Evidence map›Paper›PMID 30392076›Full record

ReviewPediatric nephrology (Berlin, Germany)2019

The role of CD47 in pathogenesis and treatment of renal ischemia reperfusion injury.

Jeffrey S Isenberg, David D Roberts

Open access · greenAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024
    Review
  6. Article
  7. Article
  8. Emerging phagocytosis checkpoints in cancer immunotherapy.Signal transduction and targeted therapy · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
  15. 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

2 authors at 2 institutions in 1 country.

Jeffrey S IsenbergDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
David D RobertsLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. droberts@mail.nih.gov.ORCID 0000-0002-2481-2981
National Institutes of Health · USUniversity of Pittsburgh · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Roles of Glycoconjugates and Redox Signaling in Tumor BiologyZIASC009174 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$4.9M
Intramural NIH HHS ZIA SC009172Intramural NIH HHS ZIA SC009174NCI NIH HHS ZIA SC 009172
6 · The paper itself

Abstract

Ischemia reperfusion (IR) injury is a process defined by the temporary loss of blood flow and tissue perfusion followed later by restoration of the same. Brief periods of IR can be tolerated with little permanent deficit, but sensitivity varies for different target cells and tissues. Ischemia reperfusion injuries have multiple causes including peripheral vascular disease and surgical interventions that disrupt soft tissue and organ perfusion as occurs in general and reconstructive surgery. Ischemia reperfusion injury is especially prominent in organ transplantation where substantial effort has been focused on protecting the transplanted organ from the consequences of IR. A number of factors mediate IR injury including the production of reactive oxygen species and inflammatory cell infiltration and activation. In the kidney, IR injury is a major cause of acute injury and secondary loss of renal function. Transplant-initiated renal IR is also a stimulus for innate and adaptive immune-mediated transplant dysfunction. The cell surface molecule CD47 negatively modulates cell and tissue responses to stress through limitation of specific homeostatic pathways and initiation of cell death pathways. Herein, a summary of the maladaptive activities of renal CD47 will be considered as well as the possible therapeutic benefit of interfering with CD47 to limit renal IR.

Indexed as

Age FactorsAnimalsAntigens, DifferentiationCD47 AntigenHumansKidneyKidney DiseasesReceptors, ImmunologicReperfusion InjurySignal TransductionAntigens, DifferentiationCD47 AntigenReceptors, ImmunologicSIRPA protein, humanCD47Ischemia reperfusion injuryKidneyRenalSIRP-αThrombospondin-1

Identifiers

PMID30392076
PMCPMC6677644
OpenAlexW2899494588

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.