Open medicine (Warsaw, Poland) · 2024
Iron in ventricular remodeling and aneurysms post-myocardial infarction.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Zuoyan, Ding Xiang, Pan Jingyu, Wang Xueyan, Lin Jieming, Wang Xinzhu
Аннотация
BACKGROUND: Post-myocardial infarction (MI) complications, including ventricular remodeling (VR) and left ventricular aneurysm (LVA) formation, significantly affect patient prognosis and quality of life. Both iron overload and deficiency play critical roles in these pathological processes.
OBJECTIVES: This review aims to explore the mechanisms linking abnormal iron metabolism with post-MI VR and LVA formation and to highlight therapeutic strategies that regulate iron levels to mitigate adverse cardiac remodeling.
METHODS: The review analyzes existing clinical and experimental research on the role of iron metabolism in post-MI complications. It focuses on iron overload, oxidative stress, ferroptosis, and the impact of iron deficiency on mitochondrial function, energy metabolism, and cardiomyocyte repair.
RESULTS: Iron overload exacerbates myocardial injury through oxidative stress, ferroptosis, and inflammation, leading to fibrosis and ventricular dilation. In contrast, iron-deficiency impairs mitochondrial function, energy metabolism, and cardiomyocyte repair, further contributing to adverse remodeling outcomes. Therapeutic strategies such as iron chelators, ferroptosis inhibitors, and iron supplementation are potential interventions for mitigating adverse remodeling.
CONCLUSION: Abnormal iron metabolism, both overload and deficiency, plays a critical role in post-MI complications. Therapeutic strategies targeting iron levels hold promise for reducing adverse cardiac remodeling and improving patient outcomes after MI.
OBJECTIVES: This review aims to explore the mechanisms linking abnormal iron metabolism with post-MI VR and LVA formation and to highlight therapeutic strategies that regulate iron levels to mitigate adverse cardiac remodeling.
METHODS: The review analyzes existing clinical and experimental research on the role of iron metabolism in post-MI complications. It focuses on iron overload, oxidative stress, ferroptosis, and the impact of iron deficiency on mitochondrial function, energy metabolism, and cardiomyocyte repair.
RESULTS: Iron overload exacerbates myocardial injury through oxidative stress, ferroptosis, and inflammation, leading to fibrosis and ventricular dilation. In contrast, iron-deficiency impairs mitochondrial function, energy metabolism, and cardiomyocyte repair, further contributing to adverse remodeling outcomes. Therapeutic strategies such as iron chelators, ferroptosis inhibitors, and iron supplementation are potential interventions for mitigating adverse remodeling.
CONCLUSION: Abnormal iron metabolism, both overload and deficiency, plays a critical role in post-MI complications. Therapeutic strategies targeting iron levels hold promise for reducing adverse cardiac remodeling and improving patient outcomes after MI.