Evidence map›Paper›PMID 23844272›Full record

ReviewOxidative medicine and cellular longevity2013

Targeting microglial K(ATP) channels to treat neurodegenerative diseases: a mitochondrial issue.

Manuel J Rodríguez, Margot Martínez-Moreno, Francisco J Ortega, Nicole Mahy

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  12. Pharmacological modulation of mitochondrial ion channels.British journal of pharmacology · 2019
    Review
  13. KMolecular neurobiology · 2018
    Article
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  17. Diazoxide attenuates autoimmune encephalomyelitis and modulates lymphocyte proliferation and dendritic cell functionality.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    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 at 3 institutions in 1 country.

Manuel J RodríguezUnitat de Bioquímica i Biologia Molecular, Facultat de Medicina, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Universitat de Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, UB, E 08036 Barcelona, Spain. marodriguez@ub.edu
Margot Martínez-Moreno
Francisco J Ortega
Nicole Mahy
Biomedical Research Networking Center on Neurodegenerative Diseases · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.

Indexed as

AnimalsHumansMicrogliaMitochondriaNeurodegenerative DiseasesPotassium Channelsmitochondrial K(ATP) channelPotassium Channels

Identifiers

PMID23844272
PMCPMC3697773
OpenAlexW2021382757

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.