Hemorrhagic Shock and Mitochondria: Pathophysiology and Therapeutic Approaches DOI Open Access
Nadezda V. Andrianova, Marina I. Buyan, Anna A. Brezgunova

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 1843 - 1843

Опубликована: Фев. 21, 2025

Severe injuries and some pathologies associated with massive bleeding, such as maternal hemorrhage, gastrointestinal perioperative rupture of an aneurysm, often lead to major blood loss the development hemorrhagic shock. A sharp decrease in circulating volume triggers a vicious cycle vasoconstriction coagulopathy leading ischemia all internal organs and, severe decompensated states, brain heart. The basis tissue damage dysfunction shock is interruption supply oxygen substrates for energy production cells, making mitochondria source target oxidative stress proapoptotic signaling. Based on these mechanisms, different strategies are proposed treat multiple organ failure that occurs main direction treatment provide cells sufficient amount utilize phosphorylation at stages increase efficiency by mitochondria. These include restoring mitochondrial complexes, example, nicotinamide adenine dinucleotide (NAD) pool. Another approaches minimize well apoptosis, which primarily dependent There also number other methods reduce improve quality population. In this review, we consider show promise therapeutic aimed bioenergetic functions cell protecting

Язык: Английский

Hemorrhagic Shock and Mitochondria: Pathophysiology and Therapeutic Approaches DOI Open Access
Nadezda V. Andrianova, Marina I. Buyan, Anna A. Brezgunova

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 1843 - 1843

Опубликована: Фев. 21, 2025

Severe injuries and some pathologies associated with massive bleeding, such as maternal hemorrhage, gastrointestinal perioperative rupture of an aneurysm, often lead to major blood loss the development hemorrhagic shock. A sharp decrease in circulating volume triggers a vicious cycle vasoconstriction coagulopathy leading ischemia all internal organs and, severe decompensated states, brain heart. The basis tissue damage dysfunction shock is interruption supply oxygen substrates for energy production cells, making mitochondria source target oxidative stress proapoptotic signaling. Based on these mechanisms, different strategies are proposed treat multiple organ failure that occurs main direction treatment provide cells sufficient amount utilize phosphorylation at stages increase efficiency by mitochondria. These include restoring mitochondrial complexes, example, nicotinamide adenine dinucleotide (NAD) pool. Another approaches minimize well apoptosis, which primarily dependent There also number other methods reduce improve quality population. In this review, we consider show promise therapeutic aimed bioenergetic functions cell protecting

Язык: Английский

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