International journal of biological macromolecules · 2026
The optineurin fatty acid-binding protein 3 axis: A novel regulator of autophagy and apoptosis in myocardial infarction.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Song Ziguang, Lu Tianyi, Yu Jiangbo, Li Zhenjun, Huang Tuo, Wang Chengcheng, Shan Gaojun, Liu Ying, Dou Boxu, Zhang Haoran, Wang Zhongyuan, Zhao Wenjie, Zhu Zixuan, Zhao Jiyi
Аннотация
BACKGROUND: Autophagy and apoptosis co-regulate the fate of cardiomyocytes after myocardial infarction (MI). OPTN is a well-characterized autophagy inducer, while FABP3 promotes apoptosis. However, the functional interaction between the two in MI remained unclear.
METHOD: A rat MI model was established by left anterior descending coronary artery ligation, with electrocardiography for model validation and echocardiography for cardiac function assessment. Molecular expression was analyzed via immunofluorescence. AC16 cardiomyocytes were subjected to oxygen-glucose deprivation (OGD), with plasmid transfection to modulate OPTN and FABP3 expression. Rapamycin (RAPA) and Baf A1 were used for autophagy modulation. Cell viability, apoptosis, protein expression, intracellular reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were measured by cellular assays.
RESULT: MI caused significant downregulation of OPTN and upregulation of FABP3 in cardiac tissue. OPTN overexpression improved cardiac function, increased left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), reduced infarct size, attenuated myocardial fibrosis and oxidative stress, and suppressed cardiomyocyte apoptosis. OPTN overexpression enhanced autophagic activity, manifested by elevated Beclin-1 and LC3I/II, alongside decreased p62. FABP3 overexpression inhibited autophagy and promoted apoptosis, counteracting the OPTN-mediated cardioprotective effect. RAPA reversed FABP3-induced injury, while Baf A1 attenuated OPTN-mediated protection. In vitro, OPTN protected cardiomyocytes by enhancing autophagic flux through reducing ROS and maintaining MMP in OGD-exposed cells.
CONCLUSION: OPTN and FABP3 formed a functional antagonistic axis in MI. OPTN exerted cardioprotective effects by enhancing autophagy, whereas FABP3 suppressed autophagy and promoted apoptosis, thereby counteracting OPTN's protective effects. Targeting OPTN/FABP3 axis to restore autophagy-apoptosis balance might be a novel therapeutic strategy.
METHOD: A rat MI model was established by left anterior descending coronary artery ligation, with electrocardiography for model validation and echocardiography for cardiac function assessment. Molecular expression was analyzed via immunofluorescence. AC16 cardiomyocytes were subjected to oxygen-glucose deprivation (OGD), with plasmid transfection to modulate OPTN and FABP3 expression. Rapamycin (RAPA) and Baf A1 were used for autophagy modulation. Cell viability, apoptosis, protein expression, intracellular reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were measured by cellular assays.
RESULT: MI caused significant downregulation of OPTN and upregulation of FABP3 in cardiac tissue. OPTN overexpression improved cardiac function, increased left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), reduced infarct size, attenuated myocardial fibrosis and oxidative stress, and suppressed cardiomyocyte apoptosis. OPTN overexpression enhanced autophagic activity, manifested by elevated Beclin-1 and LC3I/II, alongside decreased p62. FABP3 overexpression inhibited autophagy and promoted apoptosis, counteracting the OPTN-mediated cardioprotective effect. RAPA reversed FABP3-induced injury, while Baf A1 attenuated OPTN-mediated protection. In vitro, OPTN protected cardiomyocytes by enhancing autophagic flux through reducing ROS and maintaining MMP in OGD-exposed cells.
CONCLUSION: OPTN and FABP3 formed a functional antagonistic axis in MI. OPTN exerted cardioprotective effects by enhancing autophagy, whereas FABP3 suppressed autophagy and promoted apoptosis, thereby counteracting OPTN's protective effects. Targeting OPTN/FABP3 axis to restore autophagy-apoptosis balance might be a novel therapeutic strategy.