Evidence map›Paper›PMID 25902863›Full record

ArticleMolecular neurobiology2016

Activation of Autophagy Contributes to the Angiotensin II-Triggered Apoptosis in a Dopaminergic Neuronal Cell Line.

Qing Gao, Teng Jiang, Hong-Rui Zhao, Liang Wu, You-Yong Tian, Zhou Ou, Li Zhang, Yang Pan, Jie Lu, Ying-Dong Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Targeting ATScientific reports · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Roles of vascular risk factors in the pathogenesis of dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
  9. Review
  10. Article
  11. Article
  12. Article
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.

Qing GaoDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Teng JiangDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Hong-Rui ZhaoDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Liang WuDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
You-Yong TianDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China. jt870918@163.com.
Zhou OuDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Li ZhangDepartment of Neurology, Nanjing Brain Hospital, Nanjing Medical University, Nanjing, China.
Yang PanDepartment of Neurology, Nanjing Brain Hospital, Nanjing Medical University, Nanjing, China.
Jie LuDepartment of Neurology, Nanjing Brain Hospital, Nanjing Medical University, Nanjing, China.
Ying-Dong ZhangDepartment of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China. zhangyingdong@aliyun.com.
Nanjing Medical University · CNNanjing Brain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our recent study indicated that angiotensin II (Ang II), the main component of renin-angiotensin system, participated in the pathogenesis of Parkinson's disease (PD) by triggering the apoptosis of dopaminergic neuronal cells. However, the underlying mechanisms are still not fully understood. In this study, by using CATH.a cells, a dopaminergic neuronal cell line stably expressing angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R), we tested the hypothesis that activation of autophagy contributed to the apoptosis triggered by Ang II. We showed that Ang II activated autophagy and triggered apoptosis in CATH.a cells in a dose-dependent manner. More importantly, inhibition of autophagy by 3-methyladenine markedly attenuated the apoptosis caused by Ang II in CATH.a cells. In addition, the Ang II-induced autophagy and subsequent cell apoptosis could be fully abolished by an AT1R antagonist losartan rather than PD1223319, an antagonist for AT2R. Taken together, our study provides the first evidence that Ang II triggers apoptosis via activation of autophagy in a dopaminergic neuronal cell line through an AT1R-mediated manner. These findings have deepened our understanding on the role of Ang II in the pathogenesis of PD and support the use of AT1R antagonists for the treatment of this devastating neurodegenerative disease.

Indexed as

Angiotensin IIAnimalsApoptosisAutophagyCell LineDopaminergic NeuronsMiceReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Angiotensin IIReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Angiotensin IIApoptosisAutophagyParkinson’s diseaseRenin-angiotensin system

Identifiers

PMID25902863
OpenAlexW2071193552

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.