
Neurotherapeutics, Год журнала: 2025, Номер unknown, С. e00584 - e00584
Опубликована: Апрель 1, 2025
Язык: Английский
Neurotherapeutics, Год журнала: 2025, Номер unknown, С. e00584 - e00584
Опубликована: Апрель 1, 2025
Язык: Английский
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Antioxidants, Год журнала: 2025, Номер 14(3), С. 341 - 341
Опубликована: Март 14, 2025
The gasotransmitter hydrogen sulfide (H2S; also termed sulfide) generally acts as a vasodilator in the systemic vasculature but causes paradoxical constriction of pulmonary arteries (PAs). In light evidence that fall partial pressure oxygen (pO2) increases cellular levels, it was proposed rise artery smooth muscle cells (PASMCs) is responsible for hypoxic vasoconstriction, contraction PAs which develops rapidly lung regions undergoing alveolar hypoxia. contrast, hypertension (PH), sustained elevation (PAP) can develop presence diverse array pathological stimuli, including chronic hypoxia, associated with decrease expression -producing enzymes PASMCs and corresponding production by lung. Evidence PAP animal models PH be lowered administration exogenous has led to an interest using sulfide-donating agents treating this condition humans. Notably, intracellular H2S exists equilibrium other sulfur-containing species such polysulfides persulfides, these reactive sulfur are thought mediate most its effects on through persulfidation cysteine thiols proteins, leading changes function manner similar thiol oxidation species. This review sets out what currently known about mechanisms related exert their actions vascular tone, both acutely chronically, discusses potential sulfide-releasing drugs treatments different types arise
Язык: Английский
Процитировано
0Neurotherapeutics, Год журнала: 2025, Номер unknown, С. e00584 - e00584
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
0