Evidence map›Paper›PMID 29260454›Full record

ArticleThe journal of physiological sciences : JPS2018

Neuroprotective effect of treadmill exercise possibly via regulation of lysosomal degradation molecules in mice with pharmacologically induced Parkinson's disease.

Dong-Joo Hwang, Jung-Hoon Koo, Ki-Cheon Kwon, Dong-Hoon Choi, Sung-Deuk Shin, Jae-Hoon Jeong, Hyun-Seob Um, Joon-Yong Cho

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

Article in The journal of physiological sciences : JPS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
0.5field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 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 3 institutions in 1 country.

Dong-Joo HwangExercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul, 138-763, Republic of Korea.
Jung-Hoon KooExercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul, 138-763, Republic of Korea.
Ki-Cheon KwonExercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul, 138-763, Republic of Korea.
Dong-Hoon ChoiExercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul, 138-763, Republic of Korea.
Sung-Deuk ShinDepartment of Physical Education, Kyong-gi University, 600-4, Bugok-dong, Sangnok-gu, Ansan-si, Gyeonggi-do, Republic of Korea.
Jae-Hoon JeongDepartment of Physical Education, Hanyang University, 222, Wangsimni-ro, Seongdong-gu, Seoul, 04763, Republic of Korea.
Hyun-Seob UmDepartment of Exercise Prescription, Kon-Yang University, 119 Daehangro, Nonsan, Chungnam, 320-711, Republic of Korea.
Joon-Yong ChoExercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul, 138-763, Republic of Korea. chojy86@knsu.ac.kr.
Korea National Sport University · KRHanyang University · KRKyonggi University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of mitophagy, which is a selective degradation of defective mitochondria for quality control, is known to be implicated in the pathogenesis of Parkinson's disease (PD). However, how treadmill exercise (TE) regulates mitophagy-related molecules in PD remains to be elucidated. Therefore, we aimed to investigate how TE regulates α-synuclein (α-syn)-induced neurotoxicity and mitophagy-related molecules in the nigro-striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mice. Our data showed that TE exhibited a significant restoration of tyrosine hydroxylase and motor coordination with suppression of α-syn expression, hallmarks of PD, possibly via up-regulation of lysosomal degradation molecules, LAMP-2 and cathepsin L, with down-regulation of p62, LC3-II/LC3-I ratio, PINK1 and parkin in the substantia nigra of MPTP mice. Therefore, these results suggest that treadmill exercise can be used as a non-invasive intervention to improve the pathological features and maintain a healthier mitochondrial network through appropriate elimination of defective mitochondria in PD.

Indexed as

NeuroprotectionPhysical Conditioning, Animalalpha-SynucleinAnimalsBlotting, WesternCorpus StriatumGene Expression RegulationImmunohistochemistryLysosomesMiceMotor ActivityParkinsonian DisordersSubstantia NigraTyrosine 3-Monooxygenasealpha-SynucleinTyrosine 3-MonooxygenaseLysosomal degradationMitophagyParkinson’s diseasePINK1/ParkinTreadmill exerciseTyrosine hydroxylaseα-Synuclein

Identifiers

PMID29260454
PMCPMC10717095
OpenAlexW2776155482

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.