Evidence map›Paper›PMID 38336987›Full record

ReviewCurrent medical science2024

Copper Metabolism and Cuproptosis: Molecular Mechanisms and Therapeutic Perspectives in Neurodegenerative Diseases.

Xiao-Xia Ban, Hao Wan, Xin-Xing Wan, Ya-Ting Tan, Xi-Min Hu, Hong-Xia Ban, Xin-Yu Chen, Kun Huang, Qi Zhang, Kun Xiong

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
16.7field-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

27 citing papers in PubMed, 54 citations in OpenAlex.

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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

10 authors at 5 institutions in 1 country.

Xiao-Xia BanDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China.
Hao WanDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China.
Xin-Xing WanDepartment of Endocrinology, Third Xiangya Hospital, Central South University, Changsha, 430013, China.
Ya-Ting TanDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China.
Xi-Min HuDepartment of Dermatology, Xiangya Hospital, Central South University, Changsha, 430013, China.
Hong-Xia BanAffiliated Hospital, Inner Mongolia Medical University, Hohhot, 010050, China.
Xin-Yu ChenDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China.
Kun HuangDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China.
Qi ZhangDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China. zhangqi2014@csu.edu.cn.
Kun XiongDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, 430013, China. xiongkun2001@163.com.
Central South University · CNHainan Medical University · CNInner Mongolia Medical University · CNThird Xiangya Hospital · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copper is an essential trace element, and plays a vital role in numerous physiological processes within the human body. During normal metabolism, the human body maintains copper homeostasis. Copper deficiency or excess can adversely affect cellular function. Therefore, copper homeostasis is stringently regulated. Recent studies suggest that copper can trigger a specific form of cell death, namely, cuproptosis, which is triggered by excessive levels of intracellular copper. Cuproptosis induces the aggregation of mitochondrial lipoylated proteins, and the loss of iron-sulfur cluster proteins. In neurodegenerative diseases, the pathogenesis and progression of neurological disorders are linked to copper homeostasis. This review summarizes the advances in copper homeostasis and cuproptosis in the nervous system and neurodegenerative diseases. This offers research perspectives that provide new insights into the targeted treatment of neurodegenerative diseases based on cuproptosis.

Indexed as

Neurodegenerative DiseasesCell DeathCopperHumansMitochondrial ProteinsCopperMitochondrial Proteinscopper homeostasiscopper metabolismcuproptosisneurodegenerationneurodegenerative disease

Identifiers

PMID38336987
OpenAlexW4391718123

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.