What type of study is this?

This is a Animal Study study (also classified as: In Vitro Study, Observational).

August 17, 2025Frontiers in PharmacologyOpen Access

Mechanisms of sorafenib-induced cardiotoxicity: ER stress induces upregulation of ATF3, leading to downregulation of NDUFS1 expression and mitochondrial dysfunction

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Authors

MYMing Yan CPCheng Peng XLXueyan Lang

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Overview

This research reveals how sorafenib-induced cardiotoxicity activates ER stress and leads to mitochondrial dysfunction in cardiac cells, implying potential intervention targets.

Key Points

Sorafenib induces cardiotoxicity by activating ER stress, resulting in mitochondrial dysfunction and cell death.
Main finding shows significant upregulation of ATF3, linked to downregulation of NDUFS1 expression, implicating adverse cardiac effects.
The study utilized in vivo rat models and H9C2 cell-based assays, alongside biochemical validation techniques.
Modulating ATF3 could be a potential strategy for mitigating sorafenib's cardiotoxic impacts on cardiac function.

Cite This Study

Yan et al. (2025) studied this question.

synapsesocial.com/papers/68a36a360a429f797332e5ee https://doi.org/10.3389/fphar.2025.1593290

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August 17, 2025Frontiers in PharmacologyOpen Access

Mechanisms of sorafenib-induced cardiotoxicity: ER stress induces upregulation of ATF3, leading to downregulation of NDUFS1 expression and mitochondrial dysfunction

View Full Paper

Ask AI

Bookmark

Authors

MYMing Yan CPCheng Peng XLXueyan Lang

Discussion

Member takes

Overview

This research reveals how sorafenib-induced cardiotoxicity activates ER stress and leads to mitochondrial dysfunction in cardiac cells, implying potential intervention targets.

Key Points

Sorafenib induces cardiotoxicity by activating ER stress, resulting in mitochondrial dysfunction and cell death.
Main finding shows significant upregulation of ATF3, linked to downregulation of NDUFS1 expression, implicating adverse cardiac effects.
The study utilized in vivo rat models and H9C2 cell-based assays, alongside biochemical validation techniques.
Modulating ATF3 could be a potential strategy for mitigating sorafenib's cardiotoxic impacts on cardiac function.

Cite This Study

Yan et al. (2025) studied this question.

synapsesocial.com/papers/68a36a360a429f797332e5ee https://doi.org/10.3389/fphar.2025.1593290

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