Opening of the Mitochondrial Permeability Transition Pore Mediated Myocardial Damage After Perinatal Asphyxia in Neonatal Rats
Year: 2025
Type: article
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.
Source: Fetal and Pediatric Pathology
Authors: Zhixin Chen, Jianqin Chen, Yongheng Chen, Xiaoyi Fang
Language: English
Subfield: Pathology and Forensic Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Funder: Sun Yat-sen University
OpenAlex ID: W4407888304
