Opening of the Mitochondrial Permeability Transition Pore Mediated Myocardial Damage After Perinatal Asphyxia in Neonatal Rats.

IF 0.6 4区医学 Q4 PATHOLOGY Fetal and Pediatric Pathology Pub Date : 2025-05-01 Epub Date: 2025-02-24 DOI:10.1080/15513815.2025.2466804

Zhixin Chen, Jianqin Chen, Yongheng Chen, Xiaoyi Fang

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Abstract

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.

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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。

目的：探讨围产期缺氧后心肌损伤的机制。方法：建立宫内缺氧缺血模型（I/U HI）和缺氧/再氧合模型（H/R）。测定心肌损伤、线粒体功能、线粒体通透性过渡孔（MPTP）开度。结果以mean±SD表示，使用SPSS进行分析。结果：宫内缺氧诱导新生大鼠心肌损伤、线粒体功能障碍和MPTP开放。H/R导致细胞凋亡和MPTP开放。cTnI和凋亡诱导因子（AIF）水平与MPTP开放程度呈正相关。MPTP开放程度增大，Ca2+、ROS显著升高，线粒体膜电位和ATP水平降低。MPTP开放程度越大，细胞色素c和AIF释放越强。结论：MPTP开放增加可能在新生儿大鼠围产期窒息致心肌损伤中起重要作用。

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

6-12 weeks

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.