About this Research Topic
A decline in mitochondrial quality and activity is associated with normal aging and correlated with the development of a wide range of age-related diseases. Mitochondria play a major role in calcium signaling, redox stress, energy metabolism and inflammation, making this organelle a predominant cellular component that decides the fate of a cell. Multiple processes are involved in maintaining cellular mitochondrial quantity and quality, such as fission, fusion, mitophagy and mitochondrial transplantation between cells (to eliminate or replace the damaged mitochondria). Accumulating evidence proves that mitochondrial homeostasis is strongly associated with brain impairments after the occurrence of cerebrovascular diseases like ischemia stroke, subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH). Mitochondria as a therapeutic target in neuroprotection are intriguing but far from completely understood. Hence, it is crucial to uncover the specific mechanism of mitochondrial homeostasis and explore its potential influence on cerebrovascular diseases.
To further uncover the mitochondria roles in age-related cerebrovascular diseases, this research topic will focus on the following aspects:
i) Changes and the mechanisms involved in mitochondrial functions after cerebrovascular diseases occur. As is widely acknowledged, mitochondrial quality and quantity play a predominant role in injury induced oxidative stress, cell death, and neuroinflammation. Therefore, identifying and clarifying the relationship between the processes and functions could provide evidence for potential therapeutic strategies.
ii) Mechanisms of mitochondrial self-regulation. Studies report that mitochondria maintain stability by self-repairing, yet the exact mechanism remains unclear. The network of interactions between intracellular organelles is also mysterious and complex, which provides the necessary basis for understanding mitochondrial self-regulation.
iii) Mitochondria-related therapeutics. For instance, improving the cell functions through healthy mitochondria transplantation is now considered as a novel and promising treatment. Research addressing the defects of existing mitochondria-associated methods or proposing new ones are welcomed in this research topic.
In this Research Topic, we are interested in all topics associated with mitochondria and stroke, aiming to explore the pathogenesis and treatment of stroke induced brain injury from a mitochondrial perspective, covering underlying mechanisms to clinical treatment strategies.
To further uncover the mitochondria roles in age-related cerebrovascular diseases, this research topic will focus on the following aspects:
i) Changes and the mechanisms involved in mitochondrial functions after cerebrovascular diseases occur. As is widely acknowledged, mitochondrial quality and quantity play a predominant role in injury induced oxidative stress, cell death, and neuroinflammation. Therefore, identifying and clarifying the relationship between the processes and functions could provide evidence for potential therapeutic strategies.
ii) Mechanisms of mitochondrial self-regulation. Studies report that mitochondria maintain stability by self-repairing, yet the exact mechanism remains unclear. The network of interactions between intracellular organelles is also mysterious and complex, which provides the necessary basis for understanding mitochondrial self-regulation.
iii) Mitochondria-related therapeutics. For instance, improving the cell functions through healthy mitochondria transplantation is now considered as a novel and promising treatment. Research addressing the defects of existing mitochondria-associated methods or proposing new ones are welcomed in this research topic.
In this Research Topic, we are interested in all topics associated with mitochondria and stroke, aiming to explore the pathogenesis and treatment of stroke induced brain injury from a mitochondrial perspective, covering underlying mechanisms to clinical treatment strategies.
Keywords: Mitochondria, Brain injury, Stroke, Redox stress, Inflammation
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