{"title":"新生大鼠围产期窒息后线粒体通透性过渡孔开放介导的心肌损伤。","authors":"Zhixin Chen, Jianqin Chen, Yongheng Chen, Xiaoyi Fang","doi":"10.1080/15513815.2025.2466804","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>This study investigated the mechanisms underlying myocardial damage after perinatal hypoxia.</p><p><strong>Methods: </strong>An intrauterine hypoxia-ischemia model (I/U HI) and a hypoxia/reoxygenation (H/R) model were established. Myocardial damage, mitochondrial function, and mitochondria permeability transition pore (MPTP) opening were determined. The results, presented as means ± SD, were analyzed using SPSS.</p><p><strong>Results: </strong>Intrauterine hypoxia induced cardiac damage, mitochondrial dysfunction, and MPTP opening in neonatal rats. H/R led to apoptosis and MPTP opening. cTnI and apoptosis-inducing factor (AIF) levels were positively correlated with the degree of MPTP opening. The larger degree of MPTP opening combined with the significant increases in the Ca<sup>2+</sup>, ROS, and decreases in mitochondrial membrane potential and ATP levels. The larger degree of MPTP opening combined with the stronger release of cytochrome c and AIF.</p><p><strong>Conclusions: </strong>Increased MPTP opening may play a crucial role in perinatal asphyxia-induced myocardial damage in neonatal rats.</p>","PeriodicalId":50452,"journal":{"name":"Fetal and Pediatric Pathology","volume":" ","pages":"1-19"},"PeriodicalIF":0.7000,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Opening of the Mitochondrial Permeability Transition Pore Mediated Myocardial Damage After Perinatal Asphyxia in Neonatal Rats.\",\"authors\":\"Zhixin Chen, Jianqin Chen, Yongheng Chen, Xiaoyi Fang\",\"doi\":\"10.1080/15513815.2025.2466804\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>This study investigated the mechanisms underlying myocardial damage after perinatal hypoxia.</p><p><strong>Methods: </strong>An intrauterine hypoxia-ischemia model (I/U HI) and a hypoxia/reoxygenation (H/R) model were established. Myocardial damage, mitochondrial function, and mitochondria permeability transition pore (MPTP) opening were determined. The results, presented as means ± SD, were analyzed using SPSS.</p><p><strong>Results: </strong>Intrauterine hypoxia induced cardiac damage, mitochondrial dysfunction, and MPTP opening in neonatal rats. H/R led to apoptosis and MPTP opening. cTnI and apoptosis-inducing factor (AIF) levels were positively correlated with the degree of MPTP opening. The larger degree of MPTP opening combined with the significant increases in the Ca<sup>2+</sup>, ROS, and decreases in mitochondrial membrane potential and ATP levels. The larger degree of MPTP opening combined with the stronger release of cytochrome c and AIF.</p><p><strong>Conclusions: </strong>Increased MPTP opening may play a crucial role in perinatal asphyxia-induced myocardial damage in neonatal rats.</p>\",\"PeriodicalId\":50452,\"journal\":{\"name\":\"Fetal and Pediatric Pathology\",\"volume\":\" \",\"pages\":\"1-19\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2025-02-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Fetal and Pediatric Pathology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15513815.2025.2466804\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fetal and Pediatric Pathology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15513815.2025.2466804","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"PATHOLOGY","Score":null,"Total":0}
Opening of the Mitochondrial Permeability Transition Pore Mediated Myocardial Damage After Perinatal Asphyxia in Neonatal Rats.
Objectives: This study investigated the mechanisms underlying myocardial damage after perinatal hypoxia.
Methods: An intrauterine hypoxia-ischemia model (I/U HI) and a hypoxia/reoxygenation (H/R) model were established. Myocardial damage, mitochondrial function, and mitochondria permeability transition pore (MPTP) opening were determined. The results, presented as means ± SD, were analyzed using SPSS.
Results: Intrauterine hypoxia induced cardiac damage, mitochondrial dysfunction, and MPTP opening in neonatal rats. H/R led to apoptosis and MPTP opening. cTnI and apoptosis-inducing factor (AIF) levels were positively correlated with the degree of MPTP opening. The larger degree of MPTP opening combined with the significant increases in the Ca2+, ROS, and decreases in mitochondrial membrane potential and ATP levels. The larger degree of MPTP opening combined with the stronger release of cytochrome c and AIF.
Conclusions: Increased MPTP opening may play a crucial role in perinatal asphyxia-induced myocardial damage in neonatal rats.
期刊介绍：
Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports.
The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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