Cardiomyocyte‐specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia

Author:

Song Ji‐Xian12ORCID,Xu Shan123,Chen Qi12,Gou Yujing12,Zhao Chen‐Bing12,Jia Cui‐Ling12,Liu Han12,Zhang Zhi12,Li Bo‐liang12,Gao Yuhui12,Zhao Yashuo123ORCID,Ji En‐Sheng12

Affiliation:

1. Hebei Technology Innovation Center of TCM Combined Hydrogen Medicine Hebei University of Chinese Medicine Shijiazhuang China

2. Department of Physiology, Institute of Basic Medicine Hebei University of Chinese Medicine Shijiazhuang China

3. Hebei Key Laboratory of Turbidity Toxin Syndrome The First Affiliated Hospital Hebei University of Chinese Medicine Shijiazhuang China

Abstract

AbstractThe significance of iron in myocardial mitochondria function cannot be underestimated, because deviations in iron levels within cardiomyocytes may have profound detrimental effects on cardiac function. In this study, we investigated the effects of ferroportin 1 (FPN1) on cardiac iron levels and pathological alterations in mice subjected to chronic intermittent hypoxia (CIH). The cTNT‐FPN1 plasmid was administered via tail vein injection to induce the mouse with FPN1 overexpression in the cardiomyocytes. CIH was established by exposing the mice to cycles of 21%–5% FiO2 for 3 min, 8 h per day. Subsequently, the introduction of hepcidin resulted in a reduction in FPN1 expression, and H9C2 cells were used to establish an IH model to further elucidate the role of FPN1. First, FPN1 overexpression ameliorated CIH‐induced cardiac dysfunction, myocardial hypertrophy, mitochondrial damage and apoptosis. Second, FPN1 overexpression attenuated ROS levels during CIH. In addition, FPN1 overexpression mitigated CIH‐induced cardiac iron accumulation. Moreover, the administration of hepcidin resulted in a reduction in FPN1 levels, further accelerating the CIH‐induced levels of ROS, LIP and apoptosis in H9C2 cells. These findings indicate that the overexpression of FPN1 in cardiomyocytes inhibits CIH‐induced cardiac iron accumulation, subsequently reducing ROS levels and mitigating mitochondrial damage. Conversely, the administration of hepcidin suppressed FPN1 expression and worsened cardiomyocyte iron toxicity injury.

Publisher

Wiley

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