Evidence map›Paper›PMID 37358017›Full record

ArticleAging cell2023

Reduction of class I histone deacetylases ameliorates ER-mitochondria cross-talk in Alzheimer's disease.

Daniela Marinho, Ildete Luísa Ferreira, Ricardo Lorenzoni, Sandra M Cardoso, Isabel Santana, A Cristina Rego

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.4field-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

25 citing papers in PubMed, 31 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 1 country.

Daniela MarinhoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-4124-6483
Ildete Luísa FerreiraCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0001-6552-4479
Ricardo LorenzoniCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-1432-639X
Sandra M CardosoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-2199-0555
Isabel SantanaCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-8114-9434
A Cristina RegoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0003-0700-3776
University of Coimbra · PTHospitais da Universidade de Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several molecular mechanisms have been described in Alzheimer's disease (AD), including repressed gene transcription and mitochondrial and endoplasmic reticulum (ER) dysfunction. In this study, we evaluate the potential efficacy of transcriptional modifications exerted by inhibition or knockdown of class I histone deacetylases (HDACs) in ameliorating ER-mitochondria cross-talk in AD models. Data show increased HDAC3 protein levels and decreased acetyl-H3 in AD human cortex, and increased HDAC2-3 in MCI peripheral human cells, HT22 mouse hippocampal cells exposed to Aβ

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsEndoplasmic ReticulumHistone DeacetylasesHumansMiceMitochondriaAmyloid beta-PeptidesHistone Deacetylasesamyloid beta peptidecalciumhistone deacetylasesmitochondriamitochondrial-associated ER membranestacedinaline

Identifiers

PMID37358017
PMCPMC10410063
OpenAlexW4382011898

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.