Evidence map›Paper›PMID 28382594›Full record

ReviewNeurochemical research2017

The Contribution of Necroptosis in Neurodegenerative Diseases.

Lifei Shao, Shuping Yu, Wei Ji, Haizhen Li, Yilu Gao

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Mitochondrial Damage and Necroptosis in Aging Cochlea.International journal of molecular sciences · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. 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

5 authors at 2 institutions in 1 country.

Lifei ShaoDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Shuping YuDepartment of Blood Transfusion, The Forth Affiliated Hospital of Nantong University, Yancheng, 224006, Jiangsu, China.
Wei JiDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Haizhen LiMedical College, Nantong University, Nantong, 226001, Jiangsu, China.
Yilu GaoDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. ntdxgyl@163.com.
Affiliated Hospital of Nantong University · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past decades, cell apoptosis has been significantly reputed as an accidental, redundant and alternative manner of cell demise which partakes in homeostasis in the development of extensive diseases. Nevertheless, necroptosis, another novel manner of cell death through a caspase-independent way, especially in neurodegenerative diseases remains ambiguous. The cognition of this form of cell demise is helpful to understand other forms of morphological resemblance of necrosis. Additionally, the concrete signal mechanism in the regulation of necroptosis is beneficial to the diagnosis and treatment of neurodegenerative diseases. Recent studies have demonstrated that necroptotic inhibitor, 24(S)-Hydroxycholesterol and partial specific histone deacetylase inhibitors could alleviate pathogenetic conditions of neurodegenerative diseases via necroptosis pathway. In this review, we summarize recent researches about mechanisms and modulation of necroptotic signaling pathways and probe into the role of programmed necroptotic cell demise in neurodegenerative diseases such as Parkinson's disease, Multiple sclerosis, Amyotrophic lateral sclerosis.

Indexed as

AnimalsApoptosisHumansNecrosisNeurodegenerative DiseasesSignal TransductionNecroptosisNeurodegenerative diseasesRIPK1RIPK3TNF

Identifiers

PMID28382594
OpenAlexW2605049371

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.