Evidence map›Paper›PMID 28589520›Full record

ReviewNeurochemical research2018

Role of Mitochondria in Methamphetamine-Induced Dopaminergic Neurotoxicity: Involvement in Oxidative Stress, Neuroinflammation, and Pro-apoptosis-A Review.

Eun-Joo Shin, Hai-Quyen Tran, Phuong-Tram Nguyen, Ji Hoon Jeong, Seung-Yeol Nah, Choon-Gon Jang, Toshitaka Nabeshima, Hyoung-Chun Kim

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 106 citations in OpenAlex.

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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

8 authors at 5 institutions in 2 countries.

Eun-Joo ShinNeuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea.
Hai-Quyen TranNeuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea.
Phuong-Tram NguyenNeuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea.
Ji Hoon JeongDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, 06974, Republic of Korea.
Seung-Yeol NahGinsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine, Konkuk University, Seoul, 05029, Republic of Korea.
Choon-Gon JangDepartment of Pharmacology, School of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Toshitaka NabeshimaAdvanced Diagnostic System Research Laboratory, Fujita Health University Graduate School of Health Science, Toyoake, 470-1192, Japan.
Hyoung-Chun KimNeuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea. kimhc@kangwon.ac.kr.ORCID http://orcid.org/0000-0003-0420-795X
Kangwon National University · KRChung-Ang University · KRFujita Health University · JPKonkuk University · KRSungkyunkwan University · KR

Funding

Korea Food and Drug Administration #14182MFDS979National Research Foundation of Korea #NRF-2016R1A1A1A05005201National Research Foundation of Korea #NRF-2017R1A2B1003346
6 · The paper itself

Abstract

Methamphetamine (MA), an amphetamine-type psychostimulant, is associated with dopaminergic toxicity and has a high abuse potential. Numerous in vivo and in vitro studies have suggested that impaired mitochondria are critical in dopaminergic toxicity induced by MA. Mitochondria are important energy-producing organelles with dynamic nature. Evidence indicated that exposure to MA can disturb mitochondrial energetic metabolism by inhibiting the Krebs cycle and electron transport chain. Alterations in mitochondrial dynamic processes, including mitochondrial biogenesis, mitophagy, and fusion/fission, have recently been shown to contribute to dopaminergic toxicity induced by MA. Furthermore, it was demonstrated that MA-induced mitochondrial impairment enhances susceptibility to oxidative stress, pro-apoptosis, and neuroinflammation in a positive feedback loop. Protein kinase Cδ has emerged as a potential mediator between mitochondrial impairment and oxidative stress, pro-apoptosis, or neuroinflammation in MA neurotoxicity. Understanding the role and underlying mechanism of mitochondrial impairment could provide a molecular target to prevent or alleviate dopaminergic toxicity induced by MA.

Indexed as

AnimalsApoptosisCentral Nervous System StimulantsDopaminergic NeuronsHumansMethamphetamineMitochondriaOxidative StressCentral Nervous System StimulantsMethamphetamineApoptosisDopaminergic toxicityMethamphetamineMitochondriaProtein kinase Cδ

Identifiers

PMID28589520
OpenAlexW2624651707

What OpenQuestion holds

Textmetadata
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.