Fetal Cardiac Cellular Damage Caused by Anemia in Utero in Hb Bart’s Disease

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Author(s): Phudit Jatavan, Sirinart Kumfu, Theera Tongsong, Nipon Chattipakorn*

Journal Name: Current Molecular Medicine

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Background: Severe fetal anemias can cause high output cardiac failure. Mitochondria are key regulators of cardiac function. However, the effects of an early phase of fetal anemia on the fetal heart and cardiac mitochondrial function are not known.

Objective: To compare mitochondrial function and cardiac biochemical alterations in the fetal cardiac tissue between anemic and nonanemic fetuses.

Methods: A cross-sectional study was conducted in Fetuses affected by Hb Bart’s disease (n=18) and non-anemic fetuses (n=10) at 17-20 weeks. Echocardiograms had been carried out in all cases to assess prenatal cardiac function. Cardiac tissues were collected after pregnancy termination for determination of cardiac iron accumulation, mitochondrial function including mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, mitochondrial dynamics, inflammation, and apoptosis.

Results: Prenatal cardiac function evaluated by ultrasound was comparable between the Hb Bart’s and non-anemic groups. In the Bart’s group, the levels of cardiac mitochondrial depolarization and swelling, and the TNF-α level were significantly higher, compared to the nonanemic group. To the contrary, anti-inflammatory (IL-10) levels were significantly lower in the Hb Bart’s group. Additionally, active caspase3 and Bcl-2 expression were also significantly higher (P= 0.001, P=0.035) in the Bart’s group. The mitochondrial fission protein expression including p-DRP1/total DRP1 was significantly higher in the Bart’s group. However, there was no difference in cardiac iron accumulation levels between these two groups.

Conclusion: Despite equivalent prenatal cardiac function and comparable cardiac iron accumulation in the Bart’s and non-anemic groups, fetal anemia is significantly associated with cardiac mitochondrial dysfunction, increased mitochondrial fission, and increased inflammation and apoptosis. These findings indicate that an early phase of fetal anemia without cardiac iron overload can lead to cardiac mitochondrial dysfunction in fetuses with Hb Bart’s

Keywords: Anemia, apoptosis, cardiac tissue, cardiac function, fetus, hemoglobin Bart's disease, mitochondrial function, oxidative stress.

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(E-pub Ahead of Print)
DOI: 10.2174/1566524020666200610163546
Price: $95

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