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MINI REVIEW article
Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1570569
This article is part of the Research TopicCell Death Mechanisms in Neurodegenerative DisordersView all 5 articles
A review of cell death pathways in hemorrhagic stroke
Provisionally accepted- 1Neurobiology and Behavior PhD Program, Columbia University Irving Medical Center, Columbia University, New York, United States
- 2Department of Pathology & Cell Biology, Department of Neurology, The Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, Columbia University, New York, United States
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Hemorrhagic stroke is a debilitating neurological disease, affecting millions worldwide. Characterized by bleeding in the brain, it is caused by a breakdown of the blood-brain barrier (BBB) and causes damage through the presence of iron in the brain, immune activation and increased intracranial pressure. The goal of this mini-review is to explore the signaling pathways that lead to cell death that are a part of disease progression in hemorrhagic stroke. This mini-review will highlight clinical observations and data, while also incorporating findings using preclinical disease models. There are important roles for apoptosis, necroptosis, necrosis, autophagy, ferroptosis, and pyroptosis in hemorrhagic stroke. Recent work has highlighted the interplay between these phenomena, providing key regulators as potential therapeutic targets, including reactive oxygen species, iron metabolism, and caspases. Therapeutic strategies that can delay or counteract the cytotoxic effects of hemorrhage can improve clinical outcomes in hemorrhagic stroke patients.
Keywords: hemorrhagic stroke, Cell Death, Apoptosis, Inflammation, Neurovascular disease, Caspases
Received: 03 Feb 2025; Accepted: 15 Apr 2025.
Copyright: © 2025 Rinald and Troy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Carol M Troy, Department of Pathology & Cell Biology, Department of Neurology, The Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, Columbia University, New York, United States
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.