Evidence map›Paper›PMID 36922552›Full record

ArticleScientific reports2023

Mitochondrion-targeted antioxidant SkQ1 prevents rapid animal death caused by highly diverse shocks.

V P Skulachev, M Yu Vyssokikh, B V Chernyak, O A Averina, A A Andreev-Andrievskiy, R A Zinovkin, K G Lyamzaev, M V Marey, M V Egorov, O J Frolova and 3 more

Open access · goldFull text read
In one paragraph

Article in Scientific reports, 2023. 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
4.3field-weighted citation impact, top 5% 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, 28 citations in OpenAlex.

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  3. [In vitro and in vivo antibacterial effects of the mitochondrial antioxidant Visomitin againstZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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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

13 authors at 3 institutions in 2 countries.

V P SkulachevBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991. skulach@belozersky.msu.ru.
M Yu VyssokikhBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991. mikhail.vyssokikh@gmail.com.
B V ChernyakBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991. bchernyak1@gmail.com.
O A AverinaBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
A A Andreev-AndrievskiyInstitute of Mitoengineering, Lomonosov Moscow State University, Moscow, Russia, 119991.
R A ZinovkinBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
K G LyamzaevBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
M V MareyResearch Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia, 117198.
M V EgorovInstitute of Mitoengineering, Lomonosov Moscow State University, Moscow, Russia, 119991.
O J FrolovaBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
D B ZorovBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
M V SkulachevBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia, 119991.
V A SadovnichiiFaculty of Mechanics and Mathematics, Lomonosov Moscow State University, Moscow, Russia, 119991.
Lomonosov Moscow State University · RUMoscow State University · TJNational Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I.Kulakov of the Ministry of Healthcare of the Russian Federation · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The response to stress involves the activation of pathways leading either to protection from the stress origin, eventually resulting in development of stress resistance, or activation of the rapid death of the organism. Here we hypothesize that mitochondrial reactive oxygen species (mtROS) play a key role in stress-induced programmed death of the organism, which we called "phenoptosis" in 1997. We demonstrate that the synthetic mitochondria-targeted antioxidant SkQ1 (which specifically abolishes mtROS) prevents rapid death of mice caused by four mechanistically very different shocks: (a) bacterial lipopolysaccharide (LPS) shock, (b) shock in response to intravenous mitochondrial injection, (c) cold shock, and (d) toxic shock caused by the penetrating cation C

Indexed as

AntioxidantsMitochondriaAnimalsCytokinesMicePlastoquinoneReactive Oxygen SpeciesAntioxidantsCytokinesPlastoquinoneReactive Oxygen Species

Identifiers

PMID36922552
PMCPMC10017827
OpenAlexW4327676930

What OpenQuestion holds

Textfull text, public
LicenceCC BY
reference markers read1
measurements read50
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.