Evidence map›Paper›PMID 31673096›Full record

ArticleScientific reports2019

Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylate.

Hyun-Hee Park, Myung-Hoon Han, Hojin Choi, Young Joo Lee, Jae Min Kim, Jin Hwan Cheong, Je Il Ryu, Kyu-Yong Lee, Seong-Ho Koh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. 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
1.0field-weighted citation impact, top 24% 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, 29 citations in OpenAlex.

  1. Sequential-RSC pharmaceutics · 2026
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  7. Mitochondria-containing extracellular vesicles from mouse vs. human brain endothelial cells for ischemic stroke therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024
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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 1 institution in 1 country.

Hyun-Hee ParkDepartments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea.
Myung-Hoon HanDepartments of Neurosurgery, Hanyang University Guri Hospital, 11923, Guri, Korea.ORCID http://orcid.org/0000-0003-1728-5017
Hojin ChoiDepartments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea.
Young Joo LeeDepartments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea.
Jae Min KimDepartments of Neurosurgery, Hanyang University Guri Hospital, 11923, Guri, Korea.
Jin Hwan CheongDepartments of Neurosurgery, Hanyang University Guri Hospital, 11923, Guri, Korea.
Je Il RyuDepartments of Neurosurgery, Hanyang University Guri Hospital, 11923, Guri, Korea.
Kyu-Yong LeeDepartments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea. kylee@hanyang.ac.kr.
Seong-Ho KohDepartments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea. ksh213@hanyang.ac.kr.
Hanyang University Guri Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amlodipine, a L-type calcium channel blocker, has been reported to have a neuroprotective effect in brain ischemia. Mitochondrial calcium overload leads to apoptosis of cells in neurologic diseases. We evaluated the neuroprotective effects of amlodipine camsylate (AC) on neural stem cells (NSCs) injured by oxygen glucose deprivation (OGD) with a focus on mitochondrial structure and function. NSCs were isolated from rodent embryonic brains. Effects of AC on cell viability, proliferation, level of free radicals, and expression of intracellular signaling proteins were assessed in OGD-injured NSCs. We also investigated the effect of AC on mitochondrial structure in NSCs under OGD by transmission electron microscopy. AC increased the viability and proliferation of NSCs. This beneficial effect of AC was achieved by strong protection of mitochondria. AC markedly enhanced the expression of mitochondrial biogenesis-related proteins and mitochondrial anti-apoptosis proteins. Together, our results indicate that AC protects OGD-injured NSCs by protecting mitochondrial structure and function. The results of the present study provide insight into the mechanisms underlying the protective effects of AC on NSCs.

Indexed as

AmlodipineCalciumCalcium Channel BlockersEnzyme ActivationGlucoseHumansMitochondriaOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAmlodipineCalciumCalcium Channel BlockersGlucoseOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31673096
PMCPMC6823474
OpenAlexW2982439311

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.