Evidence map›Paper›PMID 27110233›Full record

ReviewEuropean surgery : ACA : Acta chirurgica Austriaca

Ischemia reperfusion-facilitated sinusoidal endothelial cell injury in liver transplantation and the resulting impact of extravasated platelet aggregation.

T Miyashita, S Nakanuma, A K Ahmed, I Makino, H Hayashi, K Oyama, H Nakagawara, H Tajima, H Takamura, I Ninomiya and 3 more

Open access · hybridAbstract readReview
In one paragraph

Review in European surgery : ACA : Acta chirurgica Austriaca. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Autophagy in liver diseases: A review.Molecular aspects of medicine · 2021
    Review
  12. Review
  13. Role of liver sinusoidal endothelial cells in liver diseases.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  14. Trained Immunity and Reactivity of Macrophages and Endothelial Cells.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Review
  15. Article
  16. Platelets Boost Recruitment of CD133International journal of molecular sciences · 2020
    Article
  17. Article
  18. Article
  19. Review
  20. Article
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

13 authors at 2 institutions in 2 countries.

T MiyashitaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
S NakanumaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
A K AhmedDepartment of Surgery, Johns Hopkins University School of Medicine, 4940 Eastern Avenue, 21224 Baltimore, MD USA.
I MakinoDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
H HayashiDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
K OyamaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
H NakagawaraDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
H TajimaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
H TakamuraDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
I NinomiyaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
S FushidaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
J W HarmonDepartment of Surgery, Johns Hopkins University School of Medicine, 4940 Eastern Avenue, 21224 Baltimore, MD USA.
T OhtaDepartment of Gastroenterological Surgery, Kanazawa University Hospital, 13-1 Takaramachi, 920-8641 Kanazawa, Ishikawa Japan.
Kanazawa University Hospital · JPJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe exact sequence of events leading to ultimate hepatocellular damage following ischemia/reperfusion (I/R) is incompletely understood. In this article, we review a mechanism of organ dysfunction after hepatic I/R or immunosuppressive treatment, in addition to the potential of liver sinusoidal endothelial cell (LSEC) protection and antiplatelet treatment for the suppression of hepatocellular damage.

methodsA review of the literature, utilizing PubMed-NCBI, was used to provide information on the components necessary for the development of hepatocellular damage following I/R.

resultsIt is well-established that LSECs damage following hepatic I/R or immunosuppressive treatment followed by extravasated platelet aggregation (EPA) is the root cause of organ dysfunction in liver transplantation. We have classified three phases, from LSECs damage to organ dysfunction, utilizing the predicted pathogenic mechanism of sinusoidal obstruction syndrome. The first phase is detachment of LSECs and sinusoidal wall destruction after LSECs injury by hepatic I/R or immunosuppressive treatment. The second phase is EPA, accomplished by sinusoidal wall destruction. The various growth factors, including thromboxane A2, serotonin, transforming growth factor-beta and plasminogen activator inhibitor-1, released by EPA in the Disse's space of zone three, induce portal hypertension and the progression of hepatic fibrosis. The third phase is organ dysfunction following portal hypertension, hepatic fibrosis, and suppressed liver regeneration through various growth factors secreted by EPA.

conclusionWe suggest that EPA in the space of Disse, initiated by LSECs damage due to hepatic I/R or immunosuppressive treatment, and activated platelets may primarily contribute to liver damage in liver transplantation. Endothelial protective therapy or antiplatelet treatment may be useful in the treatment of hepatic I/R following EPA.

Indexed as

Antiplatelet agentsEndothelial protectionExtravasated platelet aggregationIschemia/reperfusionSinusoidal endothelial damage

Identifiers

PMID27110233
PMCPMC4830883
OpenAlexW1818531370

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.