Evidence map›Paper›PMID 38689156›Full record

ArticleJournal of bioenergetics and biomembranes2024

The impact of ATP-sensitive potassium channel modulation on mitochondria in a Parkinson's disease model using SH-SY5Y cells depends on their differentiation state.

A Evinova, E Baranovicova, D Hajduchova, K Dibdiakova, I Baranova, P Racay, J Strnadel, R Pecova, E Halasova, M Pokusa

Abstract read
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. 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

10 authors.

A EvinovaBiomedical Centre Martin, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0001-5680-9616
E BaranovicovaBiomedical Centre Martin, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0003-1357-9368
D HajduchovaDepartment of Pathological Physiology, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0003-0091-0744
K DibdiakovaDepartment of Pathological Physiology, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0001-6114-4524
I BaranovaDepartment of Pathological Physiology, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0001-8273-2595
P RacayDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0003-2166-1556
J StrnadelBiomedical Centre Martin, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0002-7233-6537
R PecovaDepartment of Pathological Physiology, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0003-4257-3213
E HalasovaBiomedical Centre Martin, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia.ORCID 0000-0003-2458-1391
M PokusaBiomedical Centre Martin, Jessenius Faculty of Medicine, Comenius University, Bratislava, Slovakia. michal.pokusa@uniba.sk.ORCID 0000-0002-6313-5100

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inward rectifying potassium channels sensitive to ATP levels (KATP) have been the subject of investigation for several decades. Modulators of KATP channels are well-established treatments for metabolic as well as cardiovascular diseases. Experimental studies have also shown the potential of KATP modulation in neurodegenerative disorders. However, to date, data regarding the effects of KATP antagonists/agonists in experiments related to neurodegeneration remain inconsistent. The main source of confusion in evaluating available data seems to be the choice of experimental models. The present study aims to provide a comprehensive understanding of the effects of both opening and blocking KATP channels in two forms of SH-SY5Y cells. Our results offer valuable insights into the significance of metabolic differences between differentiated and non-differentiated SH-SY5Y cells, particularly in the context of glibenclamide and diazoxide effects under normal conditions and during the initiation of pathological events simulating Parkinson's disease in vitro. We emphasize the analysis of mitochondrial functions and changes in mitochondrial network morphology. The heightened protein expression of KATP channels identified in non-differentiated SH-SY5Y cells seems to be a platform for a more significant impact of KATP modulators in this cell type. The efficiency of rotenone treatment in inducing morphological changes in the mitochondrial network depends on the differentiation status of SH-SY5Y cells.

Indexed as

Cell DifferentiationKATP ChannelsMitochondriaCell Line, TumorDiazoxideHumansParkinson DiseaseDiazoxideKATP ChannelsDiazoxideGlibenclamideMitochondriaNeurodegenerationPotassium inward rectifying channel 6.2RotenoneSH-SY5Y

Identifiers

PMID38689156
PMCPMC11217133

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Registered trials

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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.