Evidence map›Paper›PMID 29923038›Full record

ArticleNeurochemical research2018

Ulk1/FUNDC1 Prevents Nerve Cells from Hypoxia-Induced Apoptosis by Promoting Cell Autophagy.

Li Wang, Peng Wang, He Dong, Shiduan Wang, Haichen Chu, Wei Yan, Xue Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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  15. The multi-faced role of FUNDC1 in mitochondrial events and human diseases.Frontiers in cell and developmental biology · 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

7 authors at 2 institutions in 1 country.

Li WangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Peng WangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China. wpeng118@sina.com.
He DongDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Shiduan WangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Haichen ChuDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Wei YanDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Xue ZhangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266000, China.
Qingdao University · CNAffiliated Hospital of Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell autophagy and cell apoptosis are both observed in the process of hypoxia-induced ischemic cerebral infarction (ICI). Unc-51 like autophagy activating kinase 1 (Ulk1) and FUN14 Domain-containing Protein 1 (FUNDC1) are both involved in the regulation of cell autophagy. This study aimed to investigate the regulatory effects of Ulk1 and FUNDC1 on hypoxia-induced nerve cell autophagy and apoptosis. Cell viability was measured using cell counting kit-8 (CCK-8) assay. Cell apoptosis was detected using Annexin V-PE/7-ADD staining assay. qRT-PCR was used to quantify the mRNA levels of Ulk1 and FUNDC1 in PC-12 cells. Cell transfection was performed to up-regulate the expression of Ulk1. 3-Methyladenine (3-MA) was used as autophagy inhibitor and rapamycin was used as autophagy activator in our experiments. SP600125 was used as c-Jun N-terminal kinase (JNK) inhibitor. Western blotting was performed to analyze the expression levels of key factors that are related to cell autophagy, apoptosis and JNK pathway. We found that hypoxia simultaneously induced apoptosis and autophagy of PC-12 cells. The activation of Ulk1 and FUNDC1 were also found in PC-12 cells after hypoxia induction. Overexpression of Ulk1 promoted the activation of FUNDC1 and prevented PC-12 cells from hypoxia-induced apoptosis. Suppression of Ulk1 had opposite effects. Furthermore, we also found that JNK pathway participated in the effects of Ulk1 overexpression on PC-12 cell apoptosis reduction. To conclude, Ulk1/FUNDC1 played critical regulatory roles in hypoxia-induced nerve cell autophagy and apoptosis. Overexpression of Ulk1 prevented nerve cells from hypoxia-induced apoptosis by promoting cell autophagy.

Indexed as

AnimalsApoptosisAutophagyAutophagy-Related Protein-1 HomologCell HypoxiaGene Expression RegulationMAP Kinase Signaling SystemMembrane ProteinsMitochondrial ProteinsNeuronsPC12 CellsRatsAutophagy-Related Protein-1 HomologFUNDC1 protein, ratMembrane ProteinsMitochondrial ProteinsULK1 protein, ratCell apoptosisCell autophagyFUN14 Domain-containing Protein 1Ischemic cerebral infarctionJNK pathwayUnc-51 like autophagy activating kinase 1

Identifiers

PMID29923038
OpenAlexW2808911710

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.