Evidence map›Paper›PMID 28273832›Full record

ReviewInternational journal of molecular sciences2017

More Insight into BDNF against Neurodegeneration: Anti-Apoptosis, Anti-Oxidation, and Suppression of Autophagy.

Shang-Der Chen, Chia-Lin Wu, Wei-Chao Hwang, Ding-I Yang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 3 pooled it
11.9field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 3 syntheses or guidelines pooled it, 250 citations in OpenAlex.

  1. Pooled it
  2. Benefits, side effects, and uses ofFrontiers in nutrition · 2025
    Pooled it
  3. Pooled it
  4. Article
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  9. Review
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  12. Article
  13. Neurobiophilia.Brain sciences · 2026
    Review
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55 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

Shang-Der ChenDepartment of Neurology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan. chensd@adm.cgmh.org.tw.
Chia-Lin WuProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan. ta730112@hotmail.com.
Wei-Chao HwangDepartment of Neurology, Taipei City Hospital, Taipei 11221, Taiwan. huangshiaowei@gmail.com.
Ding-I YangInstitute of Brain Science and Brain Research Center, National Yang-Ming University, Taipei 11221, Taiwan. diyang@ym.edu.tw.
National Yang Ming Chiao Tung University · TWChang Gung University · TWTaipei City Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to its well-established neurotrophic action, brain-derived neurotrophic factor (BDNF) also possesses other neuroprotective effects including anti-apoptosis, anti-oxidation, and suppression of autophagy. We have shown before that BDNF triggers multiple mechanisms to confer neuronal resistance against 3-nitropropionic acid (3-NP)-induced mitochondrial dysfunction in primary rat cortical cultures. The beneficial effects of BDNF involve the induction of anti-oxidative thioredoxin with the resultant expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) as well as erythropoietin (EPO)-dependent stimulation of sonic hedgehog (SHH). We further revealed that BDNF may bring the expression of sulfiredoxin, an ATP-dependent antioxidant enzyme, to offset mitochondrial inhibition in cortical neurons. Recently, we provided insights into another novel anti-oxidative mechanism of BDNF, which involves the augmentation of sestrin2 expression to endow neuronal resistance against oxidative stress induced by 3-NP; BDNF induction of sestrin2 entails the activation of a pathway involving nitric oxide (NO), cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG), and nuclear factor-κB (NF-κB). Apart from anti-apoptosis and anti-oxidation, we demonstrated in our most recent study that BDNF may activate the mammalian target of rapamycin (mTOR) with resultant activation of transcription factor c-Jun, thereby stimulating the expression of p62/sequestosome-1 to suppress heightened autophagy as a result of 3-NP exposure. Together, our results provide in-depth insight into multi-faceted protective mechanisms of BDNF against mitochondrial dysfunction commonly associated with the pathogenesis of many chronic neurodegenerative disorders. Delineation of the protective signaling pathways elicited by BDNF would endow a rationale to develop novel therapeutic regimens to halt or prevent the progression of neurodegeneration.

Indexed as

ApoptosisAutophagyOxidative StressAnimalsBrain-Derived Neurotrophic FactorCells, CulturedDisease Models, AnimalHumansMitochondriaNeurodegenerative DiseasesNeuronsNeuroprotective AgentsNitro CompoundsNuclear ProteinsPropionatesRNA-Binding Proteins3-nitropropionic acidBrain-Derived Neurotrophic FactorNeuroprotective AgentsNitro CompoundsNuclear ProteinsP62 protein, humanPropionatesRNA-Binding ProteinsSESN2 protein, humanSestrins3-nitropropionic acidp62reactive oxygen speciessestrin2sulfiredoxin

Identifiers

PMID28273832
PMCPMC5372561
OpenAlexW2592656360

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.