Evidence map›Paper›PMID 23093069›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2013

The dynamics of the mitochondrial organelle as a potential therapeutic target.

R Anne Stetler, Rehana K Leak, Yanqin Gao, Jun Chen

Abstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
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

60 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Antioxidants (Basel, Switzerland) · 2021
    Article
  14. Microvesicles transfer mitochondria and increase mitochondrial function in brain endothelial cells.Journal of controlled release : official journal of the Controlled Release Society · 2021
    Article
  15. Review
  16. [Annals of nuclear medicine · 2021
    Article
  17. Article
  18. Effects of O-GlcNAcylation on functional mitochondrial transfer from astrocytes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    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

4 authors.

R Anne StetlerState Key Laboratory of Medical Neurobiology and Institute of Brain Sciences, Fudan University Shanghai Medical College, Shanghai, China. stetlerra@upmc.edu
Rehana K Leak
Yanqin Gao
Jun Chen

Funding

INDUCIBLE DNA REPAIR IN CEREBRAL ISCHEMIAR01NS036736 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BENNETT, MICHAEL V L, GRAHAM, STEVEN H · 1997 to 2021
$5.4M
Neuroprotection in Models of Cerebral IschemiaR01NS045048 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2003 to 2015
$3.1M
Neuroprotective effect of HSP27 in Cerebral IschemiaR01NS056118 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2006 to 2010
$1.5M
Programmed Cell Death Induced by Cerebral IschemiaR01NS043802 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2002 to 2006
$1.4M
NINDS NIH HHS NS36736NINDS NIH HHS NS43802NINDS NIH HHS NS45048NINDS NIH HHS NS56118NINDS NIH HHS R01 NS036736NINDS NIH HHS R01 NS043802NINDS NIH HHS R01 NS045048NINDS NIH HHS R01 NS056118
6 · The paper itself

Abstract

Mitochondria play a central role in cell fate after stressors such as ischemic brain injury. The convergence of intracellular signaling pathways on mitochondria and their release of critical factors are now recognized as a default conduit to cell death or survival. Besides the individual processes that converge on or emanate from mitochondria, a mitochondrial organellar response to changes in the cellular environment has recently been described. Whereas mitochondria have previously been perceived as a major center for cellular signaling, one can postulate that the organelle's dynamics themselves affect cell survival. This brief perspective review puts forward the concept that disruptions in mitochondrial dynamics--biogenesis, clearance, and fission/fusion events--may underlie neural diseases and thus could be targeted as neuroprotective strategies in the context of ischemic injury. To do so, we present a general overview of the current understanding of mitochondrial dynamics and regulation. We then review emerging studies that correlate mitochondrial biogenesis, mitophagy, and fission/fusion events with neurologic disease and recovery. An overview of the system as it is currently understood is presented, and current assessment strategies and their limitations are discussed.

Indexed as

AnimalsBrain IschemiaHumansMembrane FusionMitochondriaMitochondrial MembranesMitochondrial ProteinsMitophagyNeurodegenerative DiseasesNeuroprotective AgentsUltrasonographyMitochondrial ProteinsNeuroprotective Agents

Identifiers

PMID23093069
PMCPMC3597376

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.