Evidence map›Paper›PMID 32210012›Full record

ArticleAntioxidants (Basel, Switzerland)2020

Astaxanthin Prevents Mitochondrial Impairment Induced by Isoproterenol in Isolated Rat Heart Mitochondria.

Olga Krestinina, Yulia Baburina, Roman Krestinin, Irina Odinokova, Irina Fadeeva, Linda Sotnikova

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-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

28 citing papers in PubMed, 52 citations in OpenAlex.

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  9. Astaxanthin Protects Against HLife (Basel, Switzerland) · 2024
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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 1 institution in 1 country.

Olga KrestininaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Yulia BaburinaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Roman KrestininInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Irina OdinokovaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Irina FadeevaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Linda SotnikovaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, 142290 Moscow region, Russia.
Institute of Theoretical and Experimental Biophysics · RU

Funding

Российский Фонд Фундаментальных Исследований (РФФИ) 20-015-00072Российский Фонд Фундаментальных Исследований (РФФИ) 20-04-00131
6 · The paper itself

Abstract

Mitochondria are considered to be a power station of the cell. It is known that they play a major role in both normal and pathological heart function. Alterations in mitochondrial bioenergetics are one of the main causes of the origin and progression of heart failure since they have an inhibitory effect on the activity of respiratory complexes in the inner mitochondrial membrane. Astaxanthin (AST) is a xanthophyll carotenoid of mainly marine origin. It has both lipophilic and hydrophilic properties and may prevent mitochondrial dysfunction by permeating the cell membrane and co-localizing within mitochondria. The carotenoid suppresses oxidative stress-induced mitochondrial dysfunction and the development of diseases. In the present study, it was found that the preliminary oral administration of AST upregulated the activity of respiratory chain complexes and ATP synthase and the level of their main subunits, thereby improving the respiration of rat heart mitochondria (RHM) in the heart injured by isoproterenol (ISO). AST decreased the level of cyclophilin D (CyP-D) and increased the level of adenine nucleotide translocase (ANT) in this condition. It was concluded that AST could be considered as a potential mitochondrial-targeted agent in the therapy of pathological conditions associated with oxidative damage and mitochondrial dysfunction. AST, as a dietary supplement, has a potential in the prevention of cardiovascular diseases.

Indexed as

ATP synthase activityisoproterenolmitochondrial respirationoxidative phosphorylationthe activity of respiratory chain complexes

Identifiers

PMID32210012
PMCPMC7139515
OpenAlexW3012776282

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.