Evidence map›Paper›PMID 28428752›Full record

ArticleFrontiers in pharmacology2017

Desensitizing Mitochondrial Permeability Transition by ERK-Cyclophilin D Axis Contributes to the Neuroprotective Effect of Gallic Acid against Cerebral Ischemia/Reperfusion Injury.

Jing Sun, Da-Dui Ren, Jin-Yi Wan, Chen Chen, Dong Chen, Huan Yang, Chun-Lai Feng, Jing Gao

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

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  10. Diplacone Isolated fromInternational journal of molecular sciences · 2023
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  13. Furanoditerpenes fromACS chemical neuroscience · 2022
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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.

Jing SunNeurobiology and Mitochondrial Key Laboratory, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Da-Dui RenNeurobiology and Mitochondrial Key Laboratory, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Jin-Yi WanDepartment of Traditional Chinese Medicine, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Chen ChenNeurobiology and Mitochondrial Key Laboratory, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Dong ChenNeurobiology and Mitochondrial Key Laboratory, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Huan YangDepartment of Traditional Chinese Medicine, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Chun-Lai FengDepartment of Pharmaceutics, School of Pharmacy, Jiangsu UniversityZhenjiang, China.
Jing GaoNeurobiology and Mitochondrial Key Laboratory, School of Pharmacy, Jiangsu UniversityZhenjiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a devastating disease with complex pathophysiology. Much evidence confirms that opening of the mitochondrial permeability transition pore (MPTP) is related with mitochondrial dysfunction to apoptosis in ischemic stroke, thus elucidating its signaling mechanism and screening novel MPTP inhibitor is therefore of paramount importance. Our earlier studies identified that gallic acid (GA), a naturally occurring plant phenol, endows with effect on inhibition of mitochondrial dysfunction, which has significant neuroprotective effect in cerebral ischemia/reperfusion injury. However, its molecular mechanisms regulating mitochondrial dysfunction remain elusive. Here, we uncover a role of GA in protecting mitochondria via MPTP inhibition. In addition to inhibit CypD binding to adenine nucleotide translocator, GA potentiates extracellular signal-regulated kinases (ERK) phosphorylation, leading to a decrease in cyclophilin D (CypD) expression, resulting in a desensitization to induction of MPTP, thus inhibiting caspase activation and ultimately giving rise to cellular survival. Our study firstly identifies ERK-CypD axis is one of the cornerstones of the cell death pathways following ischemic stroke, and confirms GA is a novel inhibitor of MPTP, which inhibits apoptosis depending on regulating the ERK-CypD axis.

Indexed as

cerebral ischemia/reperfusioncyclophilin D (CypD)extracellular signal-regulated kinases (ERK)gallic acid (GA)mitochondrial permeability transition pore (MPTP)

Identifiers

PMID28428752
PMCPMC5382198

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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.