Molecular mechanisms of interaction between ferroptosis and cuproptosis in ischemic stroke. Pharmacological perspectives on preventing brain dysfunction

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Дәйексөз келтіру

Толық мәтін

Ашық рұқсат Ашық рұқсат
Рұқсат жабық Рұқсат берілді
Рұқсат жабық Рұқсат ақылы немесе тек жазылушылар үшін

Аннотация

Ischemic stroke is one of the most severe and common neurological disorders, posing a significant threat to the health and life expectancy of affected individuals. Resulting from impaired blood flow, ischemic stroke leads to hypoxia and cerebral tissue ischemia, triggering a cascade of pathophysiological changes that markedly exacerbate neuronal damage and may ultimately result in cell death. New recent studies increasingly focus on newly discovered mechanisms of cell death, such as ferroptosis and cuproptosis. There is growing evidence supporting the independent roles of ferroptosis and cuproptosis in ischemic stroke. The aim of this review is to elucidate the potential mechanisms of cross-regulation between ferroptosis and cuproptosis and to investigate their regulatory roles in ischemic stroke. This review thoroughly examines intracellular interactions between ferroptosis and cuproptosis in ischemic stroke, emphasizing key aspects such as the fundamental roles of iron and copper, metabolic disturbances in ischemic stroke, cross-influences, and signaling pathways. Summarizing recent publications not only deepens our understanding of the pathogenesis of ischemic stroke but also suggests novel perspectives and directions for future pharmacological interventions in the treatment of ischemic stroke.

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Авторлар туралы

Vladimir Vashchenko

Kirov Military Medical Academy

Хат алмасуға жауапты Автор.
Email: vladimir-vaschenko@yandex.ru

Dr. Sci. (Biology)

Ресей, Saint Petersburg

Elena Sorokoletova

Kirov Military Medical Academy

Email: helensoroc@yandex.ru
ORCID iD: 0000-0002-9645-3391

Cand. Sci. (Biology)

Ресей, Saint Petersburg

Petr Shabanov

Kirov Military Medical Academy

Email: pdshabanov@mail.ru
ORCID iD: 0000-0003-1464-1127
SPIN-код: 8974-7477

MD, Dr. Sci. (Medicine), Professor

Ресей, Saint Petersburg

Әдебиет тізімі

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2. Fig. 1. Metabolic pathways of ferroptosis and their relationship with regulatory pathways in ischemic stroke. © Zhang et al., 2024. Adapted from [39]. Distributed under the terms of the CC-BY 4.0 license.

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3. Fig. 2. Simplified Scheme of Interaction between Ferroptosis and Cuproptosis Mechanisms: Phosphatidyl Polyunsaturated Fatty Acids (PL-PUFA); Glutathione (GSH); Glutathione Peroxidase 4 (GPX4); Ferredoxin 1 (FDX1); Dihydrolipoamide Sacetyltransferase (DLAT); Lipoic Acid (LA) ; Lipoate synthase, regulator of Krebs cycle protein lipoylation (LIAS); Phosphatidyl Ethanolamine-Polyunsaturated Fatty Acids (PE-PUFA); Nuclear Factor (p53; p21); Recombinant Solute Carrier Family 3, Member 2 (SLC3A2); Recombinant Solute Carrier Family 7, Member 11 (SLC7A11) ; Recombinant Solute Carrier Family 7 (SLC3A1); ATPase 7 (ATP7A/B) ; Acetyl-CoA (Ac-CoA); voltage-dependent anion channels (VDAC). © Chao M., et al. 2024. Adapted from [107] with modifications. Distributed under the terms of the CC-BY 4.0 license.

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4. Fig. 3. Chemical Structures of Selected Potential Ferroptosis and Cuproptosis Modulators.

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