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Journal Article Review Epublish 3 citations

PubMed: 39857442 DOI: 10.3390/antiox14010108

Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.

Antioxidants (Basel) 14(1)

Authors: Igor Belenichev, Olena Popazova, Nina Bukhtiyarova, Victor Ryzhenko, Sergii Pavlov, Elina Suprun, Valentyn Oksenych, Oleksandr Kamyshnyi

Affiliations

  • Department of Pharmacology and Medical Formulation with Course of Normal Physiology, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, Ukraine.
  • Department of Histology, Cytology and Embryology, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, Ukraine.
  • Department of Clinical Laboratory Diagnostics, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, Ukraine.
  • Department of Medical and Pharmaceutical Informatics and Advanced Technologies, Zaporizhzhia State Medical University, 69000 Zaporizhzhia, Ukraine.
  • The State Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine, 46 Academician Pavlov Street, 61076 Kharkov, Ukraine.
  • Faculty of Medicine, University of Bergen, 5020 Bergen, Norway.
  • Department of Microbiology, Virology and Immunology, I. Horbachevsky Ternopil State Medical University, 46001 Ternopil, Ukraine.

Abstract

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.

MeSH

Mitochondria, Neurodegenerative Diseases, Ischemia

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