Evidence map›Paper›PMID 27664163›Full record

ArticleJournal of molecular neuroscience : MN2017

Prevention of Cyclophilin D-Mediated mPTP Opening Using Cyclosporine-A Alleviates the Elevation of Necroptosis, Autophagy and Apoptosis-Related Markers Following Global Cerebral Ischemia-Reperfusion.

Farinoosh Fakharnia, Fariba Khodagholi, Leila Dargahi, Abolhassan Ahmadiani

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

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  17. Review
  18. Review
  19. Review
  20. The potential role of necroptosis in clinical diseases (Review).International journal of molecular medicine · 2021
    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

4 authors at 1 institution in 1 country.

Farinoosh FakharniaNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fariba KhodagholiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Leila DargahiNeuroBiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abolhassan AhmadianiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. aahmadiani@yahoo.com.
Shahid Beheshti University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrial permeability transition pore (mPTP) is a complex channel of the inner membrane, the opening of which leads to mitochondrial swelling and dissipation of mitochondrial membrane potential (MMP). Here, we aimed to evaluate the role of the cyclophilin D (CypD) as a prominent mediator of mPTP, on necroptosis and autophagy as well as apoptosis, beyond the global cerebral ischemia-reperfusion (I/R) injury. We showed that while cerebral I/R injury is accompanied by loss of MMP, mitochondrial swelling and programmed cell death, pretreatment with cyclosporine-A (CsA) as a potent inhibitor of CypD, led to partial but significant reduction in necroptosis markers, RIP1 and RIP3 as well as activity of glutamate-ammonia ligase (GLUL) and glutamate dehydrogenase 1 (GLUD1), downstream enzymes of RIP3. Administration of CsA also partially decreased autophagy associated proteins. Furthermore, we demonstrated that Bax/Bcl-2 ratio as well as caspase-3 activation, as the executioner of apoptosis, noticeably decreased by CsA pretreatment. Taken together, our results suggest that the CypD alongside the apoptosis regulation plays a partial role in inducing necroptosis and autophagy.

Indexed as

ApoptosisAutophagyAnimalsCerebral CortexCyclophilinsCyclosporineEnzyme InhibitorsGlutamate-Ammonia LigaseGlutamate DehydrogenaseMaleMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FProtein Serine-Threonine KinasesRatsCyclophilinsCyclosporineEnzyme InhibitorsGlutamate-Ammonia LigaseGlutamate DehydrogenaseMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FProtein Serine-Threonine KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, ratRipk3 protein, ratApoptosisAutophagyCerebral ischemia-reperfusionCyclosporine-AmPTPNecroptosis

Identifiers

PMID27664163
OpenAlexW2521540128

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.