Evidence map›Paper›PMID 23402031›Full record

ReviewAdvances in experimental medicine and biology2013

Complement-mediated microvascular injury leads to chronic rejection.

Mohammad A Khan, Mark R Nicolls

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
40.4field-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

26 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Airway hypoxia in lung transplantation.Current opinion in physiology · 2019
    Article
  13. Article
  14. The Emerging Importance of Non-HLA Autoantibodies in Kidney Transplant Complications.Journal of the American Society of Nephrology : JASN · 2017
    Review
  15. Article
  16. Genetic barriers in transplantation medicine.World journal of transplantation · 2016
    Review
  17. Microvascular injury after lung transplantation.Current opinion in organ transplantation · 2016
    Review
  18. Contribution of the anaphylatoxin receptors, C3aR and C5aR, to the pathogenesis of pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  19. Review
  20. 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 1 institution in 1 country.

Mohammad A KhanDivision of Pulmonary and Critical Care Medicine, Department of Medicine, VA Palo Alto/Stanford University School of Medicine, 300 Pasteur Dr A283 MC 5351, Stanford, CA 94305, USA.
Mark R Nicolls
Stanford University · US

Funding

The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2011 to 2021
$19.7M
Critical Role for Microvasculature in Airway TransplantationR01HL095686 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI NICOLLS, MARK ROBERT · 2010 to 2022
$4.7M
An Autoimmune Basis for Pulmonary Hypertension.R01HL082662 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI NICOLLS, MARK ROBERT · 2006 to 2009
$1.8M
NHLBI NIH HHS P01 HL108797NHLBI NIH HHS R01 HL082662NHLBI NIH HHS R01 HL095686
6 · The paper itself

Abstract

Microvascular loss may be an unappreciated root cause of chronic rejection for all solid organ transplants. As the only solid organ transplant that does not undergo primary systemic arterial revascularization at the time of surgery, lung transplants rely on the establishment of a microcirculation and are especially vulnerable to the effects of microvascular loss. Microangiopathy, with its attendant ischemia, can lead to tissue infarction and airway fibrosis. Maintaining healthy vasculature in lung allografts may be critical for preventing terminal airway fibrosis, also known as the bronchiolitis obliterans syndrome (BOS). BOS is the major obstacle to lung transplant success and affects up to 60% of patients surviving 5 years. The role of complement in causing acute microvascular loss and ischemia during rejection has recently been examined using the mouse orthotopic tracheal transplantation; this is an ideal model for parsing the role of airway vasculature in rejection. Prior to the development of airway fibrosis in rejecting tracheal allografts, C3 deposits on the vascular endothelium just as tissue hypoxia is first detected. With the eventual destruction of vessels, microvascular blood flow to the graft stops altogether for several days. Complement deficiency and complement inhibition lead to markedly improved tissue oxygenation in transplants, diminished airway remodeling, and accelerated vascular repair. CD4+ T cells and antibody-dependent complement activity independently mediate vascular destruction and sustained tissue ischemia during acute rejection. Consequently, interceding against complement-mediated microvascular injury with adjunctive therapy during acute rejection episodes, in addition to standard immunosuppression which targets CD4+ T cells, may help prevent the subsequent development of chronic rejection.

Indexed as

AnimalsCapillariesComplement System ProteinsEndothelium, VascularGraft RejectionHumansLung TransplantationNeovascularization, PhysiologicPulmonary CirculationComplement System Proteins

Identifiers

PMID23402031
PMCPMC4015512
OpenAlexW60155293

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.