Evidence map›Paper›PMID 35688289›Full record

ArticleNeuroscience research2022

BAX regulates dendritic spine development via mitochondrial fusion.

Qinhua Gu, Kaizheng Duan, Ronald S Petralia, Ya-Xian Wang, Zheng Li

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. 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 3 institutions in 1 country.

Qinhua GuSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
Kaizheng DuanSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
Ronald S PetraliaAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
Ya-Xian WangAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
Zheng LiSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: lizheng2@mail.nih.gov.
National Institute of Mental Health · USNational Institutes of Health · USNational Institute on Deafness and Other Communication Disorders · US

Funding

Non-apoptotic function of casapses in synapsesZIAMH002881 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI LI, ZHENG · 2009 to 2025
$18.9M
Advanced Imaging CoreZICDC000081 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI WINKLER, DENNIS · 2012 to 2025
$17.4M
Apoptotic molecules in synapse plasticityZ01MH002881 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI LI, ZHENG · 2007 to 2008
$1.1M
SYNTACTIC REPRESENTATIONSP50DC000081 · NIDCD · BOSTON UNIVERSITY MEDICAL CAMPUS · PI NAESER, MARGARET A · 1992 to 2001
$989k
Intramural NIH HHS Z01 MH002881Intramural NIH HHS ZIA MH002881Intramural NIH HHS ZIC DC000081NIDCD NIH HHS P50 DC000081
6 · The paper itself

Abstract

BAX is a Bcl-2 family protein acting on apoptosis. It also promotes mitochondrial fusion by interacting with the mitochondrial fusion protein Mitofusin (Mfn1 and Mfn2). Neuronal mitochondria are important for the development and modification of dendritic spines, which are subcellular compartments accommodating excitatory synapses in postsynaptic neurons. The abundance of dendritic mitochondria influences dendritic spine development. Mitochondrial fusion is essential for mitochondrial homeostasis. Here, we show that in the hippocampal neuron of BAX knockout mice, mitochondrial fusion is impaired, leading to decreases in mitochondrial length and total mitochondrial mass in dendrites. Notably, BAX knockout mice also have fewer dendritic spines and less cellular Adenosine 5'triphosphate (ATP) in dendrites. The spine and ATP changes are abolished by restoring mitochondria fusion via overexpressing Mfn1 and Mfn2. These findings indicate that BAX-mediated mitochondrial fusion in neurons is crucial for the development of dendritic spines and the maintenance of cellular ATP levels.

Indexed as

Dendritic SpinesMitochondrial DynamicsAdenosine TriphosphateAnimalsbcl-2-Associated X ProteinGTP PhosphohydrolasesMiceMitochondrial ProteinsAdenosine TriphosphateBax protein, mousebcl-2-Associated X ProteinGTP PhosphohydrolasesMitochondrial ProteinsATPMfnMitochondriaSpine

Identifiers

PMID35688289
PMCPMC9378631
OpenAlexW4281902397

What OpenQuestion holds

Textmetadata
LicenceTDM
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.