Evidence map›Paper›PMID 37907480›Full record

ArticleCell death discovery2023

NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway.

Kai Yang, Jue Wu, Shang Li, Shan Wang, Jing Zhang, Yi-Peng Wang, You-Sheng Yan, Hua-Ying Hu, Ming-Fang Xiong, Chao-Bo Bai and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. 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
7.9field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Molecular medicine reports · 2026
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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

15 authors at 3 institutions in 1 country.

Kai Yang *Prenatal Diagnosis Center, Beijing Obstetrics and Gynecology Hospital; Beijing Maternal and Child Health Care Hospital, Capital Medical University, Beijing, 100026, China.ORCID http://orcid.org/0000-0002-7457-3106
Jue Wu *Medical Innovation Research Division, Chinese PLA General Hospital, Beijing, 100853, China.ORCID http://orcid.org/0000-0001-6008-8428
Shang Li *Department of Anesthesiology, Peking University People's Hospital, Beijing, 100044, China.ORCID http://orcid.org/0009-0008-2121-8347
Shan WangMedical Innovation Research Division, Chinese PLA General Hospital, Beijing, 100853, China.
Jing ZhangPrenatal Diagnosis Center, Shijiazhuang Obstetrics and Gynecology Hospital, Key Laboratory of Maternal and Fetal Medicine of Hebei Province, Shijiazhuang, Hebei, 050011, China.
Yi-Peng WangPrenatal Diagnosis Center, Beijing Obstetrics and Gynecology Hospital; Beijing Maternal and Child Health Care Hospital, Capital Medical University, Beijing, 100026, China.
You-Sheng YanPrenatal Diagnosis Center, Beijing Obstetrics and Gynecology Hospital; Beijing Maternal and Child Health Care Hospital, Capital Medical University, Beijing, 100026, China.
Hua-Ying HuMedical Innovation Research Division, Chinese PLA General Hospital, Beijing, 100853, China.
Ming-Fang XiongInstitute of Hematology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, 100071, China.
Chao-Bo BaiDepartment of Neurology, Peking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing, 100191, China.
Yong-Qing SunPrenatal Diagnosis Center, Beijing Obstetrics and Gynecology Hospital; Beijing Maternal and Child Health Care Hospital, Capital Medical University, Beijing, 100026, China.
Wen-Qi ChenPrenatal Diagnosis Center, Shijiazhuang Obstetrics and Gynecology Hospital, Key Laboratory of Maternal and Fetal Medicine of Hebei Province, Shijiazhuang, Hebei, 050011, China.
Yang ZengInstitute of Hematology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, 100071, China. zengzengyang89@126.com.ORCID http://orcid.org/0000-0002-6718-9501
Jun-Liang YuanDepartment of Neurology, Peking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing, 100191, China. junliangyuan@bjmu.edu.cn.
Cheng-Hong YinPrenatal Diagnosis Center, Beijing Obstetrics and Gynecology Hospital; Beijing Maternal and Child Health Care Hospital, Capital Medical University, Beijing, 100026, China. yinchh@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-2503-3285
Capital Medical University · CNChinese PLA General Hospital · CNPeking University · CN

Funding

Beijing Nova Program Z201100006820057
6 · The paper itself

Abstract

Hippocampal neuronal damage may induce cognitive impairment. Neurotrophic tyrosine kinase receptor 1 (NTRK1) reportedly regulates neuronal damage, although the underlying mechanism remains unclear. The present study aimed to investigate the role of NTRK1 in mouse hippocampal neuronal damage and the specific mechanism. A mouse NTRK1-knockdown model was established and subjected to pre-treatment with BAY-3827, followed by a behavioral test, Nissl staining, and NeuN immunofluorescence (IF) staining to evaluate the cognitive impairment and hippocampal neuronal damage. Next, an in vitro analysis was conducted using the CCK-8 assay, TUNEL assay, NeuN IF staining, DCFH-DA staining, JC-1 staining, ATP content test, mRFP-eGFP-LC3 assay, and LC3-II IF staining to elucidate the effect of NTRK1 on mouse hippocampal neuronal activity, apoptosis, damage, mitochondrial function, and autophagy. Subsequently, rescue experiments were performed by subjecting the NTRK1-knockdown neurons to pre-treatment with O304 and Rapamycin. The AMPK/ULK1/FUNDC1 pathway activity and mitophagy were detected using western blotting (WB) analysis. Resultantly, in vivo analysis revealed that NTRK1 knockdown induced mouse cognitive impairment and hippocampal tissue damage, in addition to inactivating the AMPK/ULK1/FUNDC1 pathway activity and mitophagy in the hippocampal tissues of mice. The treatment with BAY-3827 exacerbated the mouse depressive-like behavior induced by NTRK1 knockdown. The results of in vitro analysis indicated that NTRK1 knockdown attenuated viability, NeuN expression, ATP production, mitochondrial membrane potential, and mitophagy, while enhancing apoptosis and ROS production in mouse hippocampal neurons. Conversely, pre-treatment with O304 and rapamycin abrogated the suppression of mitophagy and the promotion of neuronal damage induced upon NTRK1 silencing. Conclusively, NTRK1 knockdown induces mouse hippocampal neuronal damage through the suppression of mitophagy via inactivating the AMPK/ULK1/FUNDC1 pathway. This finding would provide insight leading to the development of novel strategies for the treatment of cognitive impairment induced due to hippocampal neuronal damage.

Identifiers

PMID37907480
PMCPMC10618268
OpenAlexW4388044405

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.