Evidence map›Paper›PMID 29900530›Full record

ArticleJournal of neurochemistry2018

Cyclophilin D regulates neuronal activity-induced filopodiagenesis by fine-tuning dendritic mitochondrial calcium dynamics.

Shaomei Sui, Jing Tian, Esha Gauba, Qi Wang, Lan Guo, Heng Du

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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 2 institutions in 2 countries.

Shaomei SuiAD Center, Department of Neurology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Jing TianDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, Texas, USA.
Esha GaubaDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, Texas, USA.
Qi WangAD Center, Department of Neurology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Lan GuoDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, Texas, USA.
Heng DuAD Center, Department of Neurology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, Shandong, China.ORCID 0000-0002-2661-5818
Shandong University · CNThe University of Texas at Dallas · US

Funding

Mitochondrial ATP Synthase Dysfunction and Synaptic Stress in Alzheimer's DiseaseR01AG053588 · NIA · UNIVERSITY OF TEXAS DALLAS · PI DU, HENG · 2016 to 2020
$1.9M
Mitochondrial pore and synaptic stress in Alzheimer's diseaseR00AG037716 · NIA · UNIVERSITY OF TEXAS DALLAS · PI DU, HENG · 2013 to 2015
$740k
NIA NIH HHS R00 AG037716NIA NIH HHS R01 AG053588
6 · The paper itself

Abstract

Recent studies have highlighted the role of mitochondria in dendritic protrusion growth and plasticity. However, the detailed mechanisms that mitochondria regulate dendritic filopodia morphogenesis remain elusive. Cyclophilin D (CypD, gene name: Ppif) controls the opening of mitochondrial permeability transition pore. Although the pathological relevance of CypD has been intensively investigated, little is known about its physiological function in neurons. Here, we have found that genetic depletion of or pharmaceutical inhibition of CypD blunts the outgrowth of dendritic filopodia in response to KCl-stimulated neuronal depolarization. Further cell biological studies suggest that such inhibitory effect of CypD loss-of-function is closely associated with compromised flexibility of dendritic mitochondrial calcium regulation during neuronal depolarization, as well as the resultant changes in intradendritic calcium homeostasis, calcium signaling activation, dendritic mitochondrial motility and redistribution. Interestingly, loss of CypD attenuates oxidative stress-induced mitochondrial calcium perturbations and dendritic protrusion injury. Therefore, our study has revealed the physiological function of CypD in dendritic plasticity by acting as a fine-tuner of mitochondrial calcium homeostasis. Moreover, CypD plays distinct roles in neuronal physiology and pathology. Cover Image for this issue: doi: 10.1111/jnc.14189.

Indexed as

AnimalsAnimals, NewbornBrainCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedCyclophilinsDendritesFemaleMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaMitochondrial DynamicsMitochondrial Membrane Transport ProteinsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2CyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitochondrial ProteinsPeptidyl-Prolyl Isomerase FPotassium ChloridePPIF protein, mousecyclophilin Ddendritic spine morphogenesisdepolarizationmitochondriamitochondrial permeability transition

Identifiers

PMID29900530
PMCPMC6107423
OpenAlexW2808595031

What OpenQuestion holds

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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.