Evidence map›Paper›PMID 28487636›Full record

ArticleFrontiers in cellular neuroscience2017

Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats.

Jing Wu, Shuangying Hao, Xiao-Ru Sun, Hui Zhang, Huihui Li, Hongting Zhao, Mu-Huo Ji, Jian-Jun Yang, Kuanyu Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. 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
3.2field-weighted citation impact, top 9% 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, 43 citations in OpenAlex.

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  7. SS-31 inhibits mtDNA-cGAS-STING signaling to improve POCD by activating mitophagy in aged mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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  20. Mitochondria-Targeted Antioxidants: A Step towards Disease Treatment.Oxidative medicine and cellular longevity · 2020
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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

9 authors at 3 institutions in 1 country.

Jing WuJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing UniversityNanjing, China.
Shuangying HaoMedical School of Henan Polytechnic UniversityJiaozuo, China.
Xiao-Ru SunDepartment of Anesthesiology, Zhongda Hospital, School of Medicine, Southeast UniversityNanjing, China.
Hui ZhangDepartment of Anesthesiology, Zhongda Hospital, School of Medicine, Southeast UniversityNanjing, China.
Huihui LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing UniversityNanjing, China.
Hongting ZhaoJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing UniversityNanjing, China.
Mu-Huo JiDepartment of Anesthesiology, Zhongda Hospital, School of Medicine, Southeast UniversityNanjing, China.
Jian-Jun YangDepartment of Anesthesiology, Zhongda Hospital, School of Medicine, Southeast UniversityNanjing, China.
Kuanyu LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing UniversityNanjing, China.
Nanjing University · CNZhongda Hospital Southeast University · CNHenan Polytechnic University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are supposed to be involved in the early pathogenesis of general anesthesia (GA)-induced neurotoxicity and long-term cognitive deficits in developing brains. However, effective pharmacologic agents targeted on mitochondria during GA exposure are lacking. This study explores the protective effects of mitochondrion-targeted antioxidant elamipretide (SS-31) on mitochondrial morphogenesis and cognition in developing rats exposed to isoflurane. Rat pups at postnatal day (PND) 7 were exposed to 1.5% isoflurane for 6 h following intraperitoneal administration of elamipretide or vehicle with 30 min interval. The hippocampus was immediately removed for biochemical assays. Histopathological studies were conducted at PND 21, and behavioral tests were performed at PND 40 or 60. We found that early exposure to isoflurane caused remarkable reactive oxygen species (ROS) accumulation, mitochondrial deformation and neuronal apoptosis in hippocampus. The injury occurrence ultimately gave rise to long-term cognitive deficits in developing rats. Interestingly, pretreatment with elamipretide not only provided protective effect against oxidative stress and mitochondrial damages, but also attenuated isoflurane-induced cognitive deficits. Our data support the notion that mitochondrial damage is an early and long lasting event of GA-induced injury and suggest that elamipretide might have clinically therapeutic benefits for pediatric patients undertaking GA.

Indexed as

antioxidantcognitionelamipretidegeneral anesthesiamitochondrial morphology

Identifiers

PMID28487636
PMCPMC5403826
OpenAlexW2608713782

What OpenQuestion holds

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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.