# Cuproptosis in stroke: focusing on pathogenesis and treatment

**Authors:** Liwei Xing, Zhifeng Wang, Zhihui Hao, Pan Pan, Aiming Yang, Jian Wang

PMC · DOI: 10.3389/fnmol.2024.1349123 · Frontiers in Molecular Neuroscience · 2024-03-28

## TL;DR

This paper reviews cuproptosis, a new type of cell death, and its potential role in stroke, focusing on how copper affects disease progression and possible treatment strategies.

## Contribution

The paper introduces cuproptosis as a novel mechanism in stroke pathogenesis and explores its connection to mitochondrial dysfunction and immune infiltration.

## Key findings

- Cuproptosis is identified as a newly discovered form of cell death linked to stroke development.
- The paper highlights the role of copper and mitochondrial dysfunction in cuproptosis-related stroke pathophysiology.
- Research suggests a need to explore cuproptosis's relationship with immune infiltration in stroke.

## Abstract

Annually, more than 15 million people worldwide suffer from stroke, a condition linked to high mortality and disability rates. This disease significantly affects daily life, impairing everyday functioning, executive function, and cognition. Moreover, stroke severely restricts patients’ ability to perform daily activities, diminishing their overall quality of life. Recent scientific studies have identified cuproptosis, a newly discovered form of cell death, as a key factor in stroke development. However, the role of cuproptosis in stroke remains unclear to researchers. Therefore, it is crucial to investigate the mechanisms of cuproptosis in stroke’s pathogenesis. This review examines the physiological role of copper, the characteristics and mechanisms of cuproptosis, the differences and similarities between cuproptosis and other cell death types, and the pathophysiology of cuproptosis in stroke, focusing on mitochondrial dysfunction and immune infiltration. Further research is necessary to understand the relationship between previous strokes and cuproptosis and to clarify the mechanisms behind these associations.

## Linked entities

- **Diseases:** stroke (MONDO:0005098)

## Full-text entities

- **Diseases:** stroke (MESH:D020521), mitochondrial dysfunction (MESH:D028361)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11007218/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC11007218/full.md

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Source: https://tomesphere.com/paper/PMC11007218