Evidence map›Paper›PMID 30501621›Full record

ReviewJournal of biomedical science2018

Mitophagy, a potential therapeutic target for stroke.

Ruiqiao Guan, Wei Zou, Xiaohong Dai, Xueping Yu, Hao Liu, Qiuxin Chen, Wei Teng

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
8.9field-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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

35 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

7 authors at 2 institutions in 2 countries.

Ruiqiao GuanHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China.
Wei ZouHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China. aiwenqiao@163.com.
Xiaohong DaiHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China.
Xueping YuHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China.
Hao LiuTonghe Hospital of Zhejiang Province, Ningbo, 315099, Zhejiang province, China.
Qiuxin ChenHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China.
Wei TengHeilongjiang University Of Chinese Medicine, Harbin, 150040, Heilongjiang province, China.
Heilongjiang University of Chinese Medicine · CNTongde Hospital of Zhejiang Province · CN

Funding

Doctoral Fund of Ministry of Education of China 20102327110003Key Program of Natural Science Foundation of Heilongjiang Province of China ZD 201204National Natural Science Foundation of China 81473764,81273824
6 · The paper itself

Abstract

Mitochondria autophagy, termed as mitophagy, is a mechanism of specific autophagic elimination of mitochondria. Mitophagy controls the quality and the number of mitochondria, eliminating dysfunctional or excessive mitochondria that can generate reactive oxygen species (ROS) and cause cell death. Mitochondria are centrally implicated in neuron and tissue injury after stroke, due to the function of supplying adenosine triphosphate (ATP) to the tissue, regulating oxidative metabolism during the pathologic process, and contribution to apoptotic cell death after stroke. As a catabolic mechanism, mitophagy links numbers of a complex network of mitochondria, and affects mitochondrial dynamic process, fusion and fission, reducing mitochondrial production of ROS, mediated by the mitochondrial permeability transition pore (MPTP). The precise nature of mitophagy's involvement in stroke, and its underlying molecular mechanisms, have yet to be fully clarified. This review aims to provide a comprehensive overview of the integration of mitochondria with mitophagy, also to introduce and discuss recent advances in the understanding of the potential role, and possible signaling pathway, of mitophagy in the pathological processes of both hemorrhagic and ischemic stroke. The author also provides evidence to explain the dual role of mitophagy in stroke.

Indexed as

AnimalsAutophagyHumansMiceMitochondriaMitophagyRatsSignal TransductionStrokeMitochondriaMitochondria autophagyStroke

Identifiers

PMID30501621
PMCPMC6271612
OpenAlexW2902832527

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.