Evidence map›Paper›PMID 38824478›Full record

ReviewApoptosis : an international journal on programmed cell death2024

Mechanisms of cuproptosis and its relevance to distinct diseases.

Qiao-Mei Lou, Fei-Fan Lai, Jing-Wei Li, Kun-Jun Mao, Hai-Tong Wan, Yu He

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2024. 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
–field-weighted citation impact
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.

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  11. Lysosome as a Chemical Reactor.International journal of molecular sciences · 2025
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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

6 authors.

Qiao-Mei LouSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Fei-Fan LaiSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Jing-Wei LiSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Kun-Jun MaoSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Hai-Tong WanSchool of Basic Medicine Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China. whtong@126.com.
Yu HeSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China. heyu0923@sina.com.

Funding

National Natural Science Foundation of China No.82374326
6 · The paper itself

Abstract

Copper is a trace element required by the organism, but once the level of copper exceeds the threshold, it becomes toxic and even causes death. The underlying mechanisms of copper-induced death are inconclusive, with different studies showing different opinions on the mechanism of copper-induced death. Multiple investigations have shown that copper induces oxidative stress, endoplasmic reticulum stress, nucleolar stress, and proteasome inhibition, all of which can result in cell death. The latest research elucidates a copper-dependent death and denominates it as cuproptosis. Cuproptosis takes place through the combination of copper and lipoylated proteins of the tricarboxylic acid cycle, triggering agglomeration of lipoylated proteins and loss of iron-sulfur cluster proteins, leading to proteotoxic stress and ultimately death. Given the toxicity and necessity of copper, abnormal levels of copper lead to diseases such as neurological diseases and cancer. The development of cancer has a high demand for copper, neurological diseases involve the change of copper contents and the binding of copper to proteins. There is a close relationship between these two kinds of diseases and copper. Here, we summarize the mechanisms of copper-related death, and the association between copper and diseases, to better figure out the influence of copper in cell death and diseases, thus advancing the clinical remedy of these diseases.

Indexed as

CopperNeoplasmsAnimalsApoptosisCell DeathEndoplasmic Reticulum StressHumansNervous System DiseasesOxidative StressCopperCancerCell deathCopperCuproptosisNeurological diseases

Identifiers

PMID38824478

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.