Evidence map›Paper›PMID 31077562›Full record

ReviewLiver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society2019

Necroptotic Cell Death in Liver Transplantation and Underlying Diseases: Mechanisms and Clinical Perspective.

Shaojun Shi, Monique M A Verstegen, Laura Mezzanotte, Jeroen de Jonge, Clemens W G M Löwik, Luc J W van der Laan

Open access · hybridAbstract readReview
In one paragraph

Review in Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society, 2019. 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
4.2field-weighted citation impact, top 6% 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, 51 citations in OpenAlex.

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  12. Targeting necroptosis in fibrosis.Molecular biology reports · 2023
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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

6 authors at 1 institution in 1 country.

Shaojun ShiDepartment of Surgery, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Monique M A VerstegenDepartment of Surgery, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Laura MezzanotteDepartment of Radiology, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Jeroen de JongeDepartment of Surgery, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Clemens W G M LöwikDepartment of Radiology, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Luc J W van der LaanDepartment of Surgery, Erasmus MC - University Medical Center, Rotterdam, the Netherlands.
Erasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell death is a natural process for the turnover of aged cells, but it can also arise as a result of pathological conditions. Cell death is recognized as a key feature in both acute and chronic hepatobiliary diseases caused by drug, alcohol, and fat uptake; by viral infection; or after surgical intervention. In the case of chronic disease, cell death can lead to (chronic) secondary inflammation, cirrhosis, and the progression to liver cancer. In liver transplantation, graft preservation and ischemia/reperfusion injury are associated with acute cell death. In both cases, so-called programmed cell death modalities are involved. Several distinct types of programmed cell death have been described of which apoptosis and necroptosis are the most well known. Parenchymal liver cells, including hepatocytes and cholangiocytes, are susceptible to both apoptosis and necroptosis, which are triggered by distinct signal transduction pathways. Apoptosis is dependent on a proteolytic cascade of caspase enzymes, whereas necroptosis induction is caspase-independent. Moreover, different from the "silent" apoptotic cell death, necroptosis can cause a secondary inflammatory cascade, so-called necroinflammation, triggered by the release of various damage-associated molecular patterns (DAMPs). These DAMPs activate the innate immune system, leading to both local and systemic inflammatory responses, which can even cause remote organ failure. Therapeutic targeting of necroptosis by pharmacological inhibitors, such as necrostatin-1, shows variable effects in different disease models.

Indexed as

AnimalsDisease Models, AnimalEnd Stage Liver DiseaseGraft RejectionHepatocytesHumansImidazolesIndolesLiverLiver TransplantationNecroptosisImidazolesIndolesnecrostatin-1

Identifiers

PMID31077562
PMCPMC6617733
OpenAlexW2944424799

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.