Evidence map›Paper›PMID 40905146›Full record

ArticleCNS neuroscience & therapeutics2025

Reorganization of Mitochondrial Function and Architecture in Response to Plant-Derived Alkaloids: Anatabine, Anabasine, and Nicotine, Investigated in SH-SY5Y Cells and in a Cellular Model of Parkinson's Disease.

Dominika Malińska, Karolina Drabik, Bernadeta Michalska, Jarosław Walczak, Małgorzata Partyka, Monika Prill, Jędrzej Szymański, Paulina Patalas-Krawczyk, Karolina Piecyk, Jerzy Duszyński and 2 more

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Dominika MalińskaNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.ORCID 0000-0002-0526-7914
Karolina DrabikNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Bernadeta MichalskaNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Jarosław WalczakNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Małgorzata PartykaNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Monika PrillNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Jędrzej SzymańskiNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Paulina Patalas-KrawczykNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Karolina PiecykNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Jerzy DuszyńskiNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Mariusz R WięckowskiNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Joanna SzczepanowskaNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.

Funding

Philip Morris International
6 · The paper itself

Abstract

aimsNicotine, anatabine, and anabasine are the most prevalent alkaloids in Nicotiana species. While nicotine is the main addictive ingredient in tobacco products, it was also shown to have neuroprotective properties. Mitochondria appear to be one of the targets of nicotine in the cell. These multifunctional organelles are also the first responders to various cellular stresses. Thus, we characterized the impact of tobacco alkaloids on these organelles.

methodsWe investigated the effects of structurally similar alkaloids, anatabine, anabasine, and nicotine, on mitochondrial function in SH-SY5Y neuroblastoma cells under basal conditions and in the presence of rotenone, a mitochondrial stressor commonly used to model the cellular pathology underlying Parkinson's disease.

resultsWe observed changes in mitochondrial behavior, including hyperpolarization, alterations in mitochondrial network morphology, increased mitochondrial turnover rates, and upregulation of mitochondrial biogenesis regulators. The profiles of changes induced by particular alkaloids slightly differed; however, they shared many features with the stress response observed upon treatment with rotenone. Interestingly, the effects of the alkaloids and rotenone were not additive. Moreover, some parameters altered by rotenone were normalized upon cotreatment with the alkaloids.

conclusionsThe results indicate that the investigated alkaloids stimulate mitochondrial stress adaptation. Despite structural similarity, they act through slightly different mechanisms.

Indexed as

AlkaloidsMitochondriaNicotineParkinson DiseasePyridinesCell Line, TumorHumansMembrane Potential, MitochondrialRotenoneAlkaloidsanatabineNicotinePyridinesRotenoneanabasineanatabinemitochondriamitochondrial remodelingnicotine

Identifiers

PMID40905146
PMCPMC12409299

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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.