Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity.

Details

Serval ID
serval:BIB_01B9FD89D57C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity.
Journal
Scientific reports
Author(s)
Rodius S., de Klein N., Jeanty C., Sánchez-Iranzo H., Crespo I., Ibberson M., Xenarios I., Dittmar G., Mercader N., Niclou S.P., Azuaje F.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Publication state
Published
Issued date
19/02/2020
Peer-reviewed
Oui
Volume
10
Number
1
Pages
2896
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Myocardial infarction (MI) is a leading cause of death worldwide. Reperfusion is considered as an optimal therapy following cardiac ischemia. However, the promotion of a rapid elevation of O <sub>2</sub> levels in ischemic cells produces high amounts of reactive oxygen species (ROS) leading to myocardial tissue injury. This phenomenon is called ischemia reperfusion injury (IRI). We aimed at identifying new and effective compounds to treat MI and minimize IRI. We previously studied heart regeneration following myocardial injury in zebrafish and described each step of the regeneration process, from the day of injury until complete recovery, in terms of transcriptional responses. Here, we mined the data and performed a deep in silico analysis to identify drugs highly likely to induce cardiac regeneration. Fisetin was identified as the top candidate. We validated its effects in an in vitro model of MI/IRI in mammalian cardiac cells. Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation - reoxygenation. It inhibits apoptosis, decreases ROS generation and caspase activation and protects from DNA damage. Interestingly, fisetin also activates genes involved in cell proliferation. Fisetin is thus a highly promising candidate drug with clinical potential to protect from ischemic damage following MI and to overcome IRI.
Pubmed
Open Access
Yes
Create date
27/02/2020 16:10
Last modification date
25/11/2020 6:25
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