Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions
The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology of various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation of reactive oxygen species (ROS), calcium homeost...
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| Format: | Article |
| Language: | English |
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MDPI AG
2025-01-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/14/1/108 |
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| author | Igor Belenichev Olena Popazova Nina Bukhtiyarova Victor Ryzhenko Sergii Pavlov Elina Suprun Valentyn Oksenych Oleksandr Kamyshnyi |
| author_facet | Igor Belenichev Olena Popazova Nina Bukhtiyarova Victor Ryzhenko Sergii Pavlov Elina Suprun Valentyn Oksenych Oleksandr Kamyshnyi |
| author_sort | Igor Belenichev |
| collection | DOAJ |
| description | The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology of various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation of reactive oxygen species (ROS), calcium homeostasis, and the execution of apoptotic processes. Disruptions in mitochondrial function, driven by factors such as oxidative stress, excitotoxicity, and altered ion balance, lead to neuronal death and contribute to cognitive impairments in several brain diseases. Mitochondrial dysfunction can arise from genetic mutations, ischemic events, hypoxia, and other environmental factors. This article highlights the critical role of mitochondrial dysfunction in the progression of neurodegenerative diseases and discusses the need for targeted therapeutic strategies to attenuate cellular damage, restore mitochondrial function, and enhance neuroprotection. |
| format | Article |
| id | doaj-art-6764724699914da8a0df6aea89cd043a |
| institution | Kabale University |
| issn | 2076-3921 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj-art-6764724699914da8a0df6aea89cd043a2025-01-24T13:19:30ZengMDPI AGAntioxidants2076-39212025-01-0114110810.3390/antiox14010108Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological InterventionsIgor Belenichev0Olena Popazova1Nina Bukhtiyarova2Victor Ryzhenko3Sergii Pavlov4Elina Suprun5Valentyn Oksenych6Oleksandr Kamyshnyi7Department of Pharmacology and Medical Formulation with Course of Normal Physiology, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, UkraineDepartment of Histology, Cytology and Embryology, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, UkraineDepartment of Clinical Laboratory Diagnostics, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, UkraineDepartment of Medical and Pharmaceutical Informatics and Advanced Technologies, Zaporizhzhia State Medical University, 69000 Zaporizhzhia, UkraineDepartment of Clinical Laboratory Diagnostics, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, UkraineThe State Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine, 46 Academician Pavlov Street, 61076 Kharkov, UkraineFaculty of Medicine, University of Bergen, 5020 Bergen, NorwayDepartment of Microbiology, Virology and Immunology, I. Horbachevsky Ternopil State Medical University, 46001 Ternopil, UkraineThe study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology of various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation of reactive oxygen species (ROS), calcium homeostasis, and the execution of apoptotic processes. Disruptions in mitochondrial function, driven by factors such as oxidative stress, excitotoxicity, and altered ion balance, lead to neuronal death and contribute to cognitive impairments in several brain diseases. Mitochondrial dysfunction can arise from genetic mutations, ischemic events, hypoxia, and other environmental factors. This article highlights the critical role of mitochondrial dysfunction in the progression of neurodegenerative diseases and discusses the need for targeted therapeutic strategies to attenuate cellular damage, restore mitochondrial function, and enhance neuroprotection.https://www.mdpi.com/2076-3921/14/1/108mitochondrial dysfunctionROScerebral ischemiaHIF-1HSP70 |
| spellingShingle | Igor Belenichev Olena Popazova Nina Bukhtiyarova Victor Ryzhenko Sergii Pavlov Elina Suprun Valentyn Oksenych Oleksandr Kamyshnyi Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions Antioxidants mitochondrial dysfunction ROS cerebral ischemia HIF-1 HSP70 |
| title | Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions |
| title_full | Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions |
| title_fullStr | Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions |
| title_full_unstemmed | Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions |
| title_short | Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions |
| title_sort | targeting mitochondrial dysfunction in cerebral ischemia advances in pharmacological interventions |
| topic | mitochondrial dysfunction ROS cerebral ischemia HIF-1 HSP70 |
| url | https://www.mdpi.com/2076-3921/14/1/108 |
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