Evidence map›Paper›PMID 30120245›Full record

ArticleExperimental & molecular medicine2018

Cell-penetrating artificial mitochondria-targeting peptide-conjugated metallothionein 1A alleviates mitochondrial damage in Parkinson's disease models.

Young Cheol Kang, Minuk Son, Sora Kang, Suyeol Im, Ying Piao, Kwang Suk Lim, Min-Young Song, Kang-Sik Park, Yong-Hee Kim, Youngmi Kim Pak

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 72 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

10 authors at 2 institutions in 1 country.

Young Cheol KangDepartment of Neuroscience, Graduate School, Kyung Hee University, Seoul, 02447, Korea.
Minuk SonDepartment of Neuroscience, Graduate School, Kyung Hee University, Seoul, 02447, Korea.
Sora KangDepartment of Neuroscience, Graduate School, Kyung Hee University, Seoul, 02447, Korea.
Suyeol ImDepartment of Neuroscience, Graduate School, Kyung Hee University, Seoul, 02447, Korea.
Ying PiaoDepartment of Physiology, College of Medicine, Kyung Hee University, Seoul, 02447, Korea.
Kwang Suk LimDepartment of Bioengineering, Institute for Bioengineering and Biopharmaceutical Research, Hanyang University, Seoul, 133-791, Korea.
Min-Young SongDepartment of Physiology, College of Medicine, Kyung Hee University, Seoul, 02447, Korea.
Kang-Sik ParkDepartment of Physiology, College of Medicine, Kyung Hee University, Seoul, 02447, Korea.
Yong-Hee KimDepartment of Bioengineering, Institute for Bioengineering and Biopharmaceutical Research, Hanyang University, Seoul, 133-791, Korea.
Youngmi Kim PakDepartment of Neuroscience, Graduate School, Kyung Hee University, Seoul, 02447, Korea. ykpak@khu.ac.kr.
Kyung Hee University · KRHanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An excess of reactive oxygen species (ROS) relative to the antioxidant capacity causes oxidative stress, which plays a role in the development of Parkinson's disease (PD). Because mitochondria are both sites of ROS generation and targets of ROS damage, the delivery of antioxidants to mitochondria might prevent or alleviate PD. To transduce the antioxidant protein human metallothionein 1A (hMT1A) into mitochondria, we computationally designed a cell-penetrating artificial mitochondria-targeting peptide (CAMP). The recombinant CAMP-conjugated hMT1A fusion protein (CAMP-hMT1A) successfully localized to the mitochondria. Treating a cell culture model of PD with CAMP-hMT1A restored tyrosine hydroxylase expression and mitochondrial activity and reduced ROS production. Furthermore, injection of CAMP-hMT1A into the brain of a mouse model of PD rescued movement impairment and dopaminergic neuronal degeneration. CAMP-hMT1A delivery into mitochondria might be therapeutic against PD by alleviating mitochondrial damage, and we predict that CAMP could be used to deliver other cargo proteins to the mitochondria.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmino Acid SequenceAnimalsCell DeathCell Line, TumorCell-Penetrating PeptidesComputer SimulationDisease Models, AnimalGreen Fluorescent ProteinsHumansMetallothioneinMiceMitochondriaNeuronsParkinson DiseaseProtein Transport1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineCell-Penetrating Peptidesenhanced green fluorescent proteinGreen Fluorescent ProteinsMetallothioneinMT1A protein, humanRecombinant Fusion ProteinsTyrosine 3-Monooxygenase

Identifiers

PMID30120245
PMCPMC6098059
OpenAlexW2887185609

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.