Evidence map›Paper›PMID 18637518›Full record

ReviewCurrent topics in microbiology and immunology2008

Mechanisms of cytomegalovirus-accelerated vascular disease: induction of paracrine factors that promote angiogenesis and wound healing.

D N Streblow, J Dumortier, A V Moses, S L Orloff, J A Nelson

Abstract readReview
In one paragraph

Review in Current topics in microbiology and immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
46.4field-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

66 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Mapping CMV-related immune signatures in blood, aorta and perivascular mediastinal adipose tissue.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Overview of Human Cytomegalovirus Pathogenesis.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  10. Review
  11. Article
  12. Rodent Models of Congenital Cytomegalovirus Infection.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  13. Review
  14. Review
  15. Control of Immediate Early Gene Expression for Human Cytomegalovirus Reactivation.Frontiers in cellular and infection microbiology · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

6 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

5 authors at 1 institution in 1 country.

D N StreblowVaccine and Gene Therapy Institute and Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, OR 97201, USA. streblow@ohsu.edu
J Dumortier
A V Moses
S L Orloff
J A Nelson
Oregon Health & Science University · US

Funding

MOLECULAR ASPECTS OF CYTOMEGALOVIRUS LATENCYR01AI021640 · NIAID · UNIVERSITY OF GUELPH · PI Meaghan H Hancock · 1985 to 2026
$8.1M
Molecular Aspects of Cytomegalovirus LatencyR37AI021640 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI HANCOCK, MEAGHAN H · 2018 to 2024
$4.0M
The role of CMV secretome in the acceleration of transplant vascular sclerosisR01HL088603 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI NELSON, JAY A · 2008 to 2012
$3.6M
CHEMOKINE RECEPTORS IN VASCULAR DISEASER01HL065754 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI NELSON, JAY A · 2000 to 2007
$2.7M
Cytomegalovirus Chemokine Receptors in Transplant Vascular SclerosisR01HL085451 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ORLOFF, SUSAN L · 2009 to 2013
$2.2M
Cellular Basis of CMV Accelerated VasculopathyR01HL071695 · NHLBI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI NELSON, JAY A · 2002 to 2005
$1.5M
Mechanisms of CMV latency in accelerated vascular diseaseR01HL083194 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI STREBLOW, DANIEL N · 2006 to 2010
$1.5M
VIRAL CHEMOKINE RECEPTORS: TRANSPLANT VASCULAR SCLEROSISR01HL066238 · NHLBI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI ORLOFF, SUSAN L · 2001 to 2003
$793k
NHLBI NIH HHS HL083194NHLBI NIH HHS HL65754NHLBI NIH HHS HL 66238-01NHLBI NIH HHS HL71695NHLBI NIH HHS R01 HL065754NHLBI NIH HHS R01 HL066238NHLBI NIH HHS R01 HL071695NHLBI NIH HHS R01 HL083194NHLBI NIH HHS R01 HL085451NHLBI NIH HHS R01 HL088603NIAID NIH HHS AI21640NIAID NIH HHS R01 AI021640NIAID NIH HHS R37 AI021640
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is associated with the acceleration of a number of vascular diseases such as atherosclerosis, restenosis, and transplant vascular sclerosis (TVS). All of these diseases are the result of either mechanical or immune-mediated injury followed by inflammation and subsequent smooth muscle cell (SMC) migration from the vessel media to the intima and proliferation that culminates in vessel narrowing. A number of epidemiological and animal studies have demonstrated that CMV significantly accelerates TVS and chronic rejection (CR) in solid organ allografts. In addition, treatment of human recipients and animals alike with the antiviral drug ganciclovir results in prolonged survival of the allograft, indicating that CMV replication is a requirement for acceleration of disease. However, although virus persists in the allograft throughout the course of disease, the number of directly infected cells does not account for the global effects that the virus has on the acceleration of TVS and CR. Recent investigations of up- and downregulated cellular genes in infected allografts in comparison to native heart has demonstrated that rat CMV (RCMV) upregulates genes involved in wound healing (WH) and angiogenesis (AG). Consistent with this result, we have found that supernatants from HCMV-infected cells (HCMV secretome) induce WH and AG using in vitro models. Taken together, these findings suggest that one mechanism for HCMV acceleration of TVS is mediated through induction of secreted cytokines and growth factors from virus-infected cells that promote WH and AG in the allograft, resulting in the acceleration of TVS. We review here the ability of CMV infection to alter the local environment by producing cellular factors that act in a paracrine fashion to enhance WH and AG processes associated with the development of vascular disease, which accelerates chronic allograft rejection.

Indexed as

AnimalsCytokinesCytomegalovirusCytomegalovirus InfectionsHumansIntercellular Signaling Peptides and ProteinsRatsSclerosisVascular DiseasesCytokinesIntercellular Signaling Peptides and Proteins

Identifiers

PMID18637518
PMCPMC2699259
OpenAlexW125742586

What OpenQuestion holds

Textmetadata
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.