Thyroxine Alleviates Energy Failure, Prevents Myocardial Cell Apoptosis, and Protects against Doxorubicin-Induced Cardiac Injury and Cardiac Dysfunction via the LKB1AMPKmTOR Axis in Mice

المؤلفون المشاركون

Wang, Yuan
Zhu, Shan
Liu, Hongtao
Wei, Wen
Tu, Yi
Chen, Chuang
Song, Junlong
Li, Juanjuan
Sun, Shengrong
Wang, Changhua
Xu, Zhiliang

المصدر

Disease Markers

العدد

المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-10، 10ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2019-12-18

دولة النشر

مصر

عدد الصفحات

10

التخصصات الرئيسية

الأمراض

الملخص EN

Background.

Previous studies have demonstrated that energy failure is closely associated with cardiac injury.

Doxorubicin (DOX) is a commonly used clinical chemotherapy drug that can mediate cardiac injury through a variety of mechanisms.

Thyroxine is well known to play a critical role in energy generation; thus, this study is aimed at investigating whether thyroxine can attenuate DOX-induced cardiac injury by regulating energy generation.

Methods.

First, the effect of DOX on adenosine diphosphate (ADP) and adenosine triphosphate (ATP) ratios in mice was assessed.

In addition, thyroxine was given to mice before they were treated with DOX to investigate the effects of thyroxine on DOX-induced cardiac injury.

Furthermore, to determine whether the liver kinase b1 (LKB1)/adenosine 5′-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) axis mediated the effect of thyroxine on DOX-induced cardiac injury, thyroxine was given to DOX-treated LKB1 knockout (KO) mice.

Results.

DOX treatment time- and dose-dependently increased the ADP/ATP ratio.

Thyroxine treatment also reduced lactate dehydrogenase (LDH) and creatine kinase myocardial band (CK-MB) levels in both serum and heart tissue and alleviated cardiac dysfunction in DOX-treated mice.

Furthermore, thyroxine reversed DOX-induced reductions in LKB1 and AMPK phosphorylation; mitochondrial complex I, III, and IV activity; and mitochondrial swelling and reversed DOX-induced increases in mTOR pathway phosphorylation and myocardial cell apoptosis.

These effects of thyroxine on DOX-treated mice were significantly attenuated by LKB1 KO.

Conclusions.

Thyroxine alleviates energy failure, reduces myocardial cell apoptosis, and protects against DOX-induced cardiac injury via the LKB1/AMPK/mTOR axis in mice.

Thyroxine may be a new agent for the clinical prevention of cardiac injury in tumor patients undergoing chemotherapy with DOX.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Wang, Yuan& Zhu, Shan& Liu, Hongtao& Wei, Wen& Tu, Yi& Chen, Chuang…[et al.]. 2019. Thyroxine Alleviates Energy Failure, Prevents Myocardial Cell Apoptosis, and Protects against Doxorubicin-Induced Cardiac Injury and Cardiac Dysfunction via the LKB1AMPKmTOR Axis in Mice. Disease Markers،Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1147718

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Wang, Yuan…[et al.]. Thyroxine Alleviates Energy Failure, Prevents Myocardial Cell Apoptosis, and Protects against Doxorubicin-Induced Cardiac Injury and Cardiac Dysfunction via the LKB1AMPKmTOR Axis in Mice. Disease Markers No. 2019 (2019), pp.1-10.
https://search.emarefa.net/detail/BIM-1147718

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Wang, Yuan& Zhu, Shan& Liu, Hongtao& Wei, Wen& Tu, Yi& Chen, Chuang…[et al.]. Thyroxine Alleviates Energy Failure, Prevents Myocardial Cell Apoptosis, and Protects against Doxorubicin-Induced Cardiac Injury and Cardiac Dysfunction via the LKB1AMPKmTOR Axis in Mice. Disease Markers. 2019. Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1147718

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1147718