Evidence map›Paper›PMID 37341832›Full record

ArticleCellular and molecular neurobiology2023

Autophagy Suppresses Ferroptosis by Degrading TFR1 to Alleviate Cognitive Dysfunction in Mice with SAE.

Lixia Du, You Wu, Qi Jia, Jin Li, Yi Li, Hongwei Ma, Zhongmin Fan, Xiaofeng Guo, Ling Li, Yuliang Peng and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Ferroptosis inhibitors: past, present and future.Frontiers in pharmacology · 2024
    Review
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  16. 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

13 authors at 2 institutions in 1 country.

Lixia Du *Department of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0003-1560-2517
You Wu *Department of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0002-9417-9712
Qi Jia *Department of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0003-3642-1387
Jin Li *Department of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0002-4593-0389
Yi LiDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0001-7165-7251
Hongwei MaDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0003-4929-3222
Zhongmin FanDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0002-3816-4284
Xiaofeng GuoDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0001-6312-835X
Ling LiDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0003-4177-4152
Yuliang PengDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0001-9736-8909
Jing LiDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.ORCID http://orcid.org/0000-0003-1446-1142
Zongping FangDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China. zongping03@163.com.ORCID http://orcid.org/0000-0002-1887-6452
Xijing ZhangDepartment of Anesthesiology and Perioperative Medicine and Department of Intensive Care Unit, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China. xjzhang0806@163.com.ORCID http://orcid.org/0000-0001-8719-1142
Xijing Hospital · CNNorthwest University · CN

Funding

Discipline Boost Program of the First Affiliated Hospital of Air Force Military Medical University No. XJZT21J08National Natural Science Foundation Grant No. 81871603National Natural Science Foundation of China no. 82171322Natural Science Foundation of Shaanxi Province of China no. 2022KJXX-102
6 · The paper itself

Abstract

Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis that is characterized by long-term cognitive impairment, which imposes a heavy burden on families and society. However, its pathological mechanism has not been elucidated. Ferroptosis is a novel form of programmed cell death that is involved in multiple neurodegenerative diseases. In the current study, we found that ferroptosis also participated in the pathological process of cognitive dysfunction in SAE, while Liproxstatin-1 (Lip-1) effectively inhibited ferroptosis and alleviated cognitive impairment. Additionally, since an increasing number of studies have suggested the crosstalk between autophagy and ferroptosis, we further proved the essential role of autophagy in this process and demonstrated the key molecular mechanism of the autophagy-ferroptosis interaction. Currently, we showed that autophagy in the hippocampus was downregulated within 3 days of lipopolysaccharide injection into the lateral ventricle. Moreover, enhancing autophagy ameliorated cognitive dysfunction. Importantly, we found that autophagy suppressed ferroptosis by downregulating transferrin receptor 1 (TFR1) in the hippocampus, thereby alleviating cognitive impairment in mice with SAE. In conclusion, our findings indicated that hippocampal neuronal ferroptosis is associated with cognitive impairment. In addition, enhancing autophagy can inhibit ferroptosis via degradation of TFR1 to ameliorate cognitive impairment in SAE, which shed new light on the prevention and therapy for SAE.

Indexed as

Cognitive DysfunctionFerroptosisSepsis-Associated EncephalopathyAnimalsAutophagyMiceReceptors, TransferrinReceptors, TransferrinTfrc protein, mouseAutophagyCognitive impairmentFerroptosisSepsis-associated encephalopathyTFR1

Identifiers

PMID37341832
PMCPMC11410008
OpenAlexW4381469192

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.