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Heart and Vessels
Erschienen in: Heart and Vessels 3/2023

07.11.2022 | Original Article

TRAIL inhibition by soluble death receptor 5 protects against acute myocardial infarction in rats

verfasst von: Mingli Wang, Yinxiang Wei, Xuance Wang, Fanni Ma, Weina Zhu, Xi Chen, Xiaoming Zhong, Shulian Li, Jun Zhang, Guangchao Liu, Yaohui Wang, Yuanfang Ma

Erschienen in: Heart and Vessels | Ausgabe 3/2023

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Abstract

Acute myocardial infarction (AMI) is associated with high morbidity and mortality. An effective therapeutic strategy is to rescue cardiomyocytes from death. Apoptosis is a key reason of cardiomyocyte death that can be prevented. In this study, we investigated the role of TNF-related apoptosis-inducing ligand (TRAIL) in initiating apoptosis by binding to death receptor 5 (DR5), and this procession is inhibited by soluble DR5 (sDR5) in rats after AMI. First, we found that the level of TRAIL in serum was down-regulated in AMI patients. Then, TRAIL and DR5 expression was analysed in the myocardium of rats after AMI, and their expression was up-regulated. sDR5 treatment reduced the myocardial infarct size and the levels of CK-MB and cTn-I in serum. The expression of caspase 3 and PARP is decreased, but the anti-apoptotic factor Bcl-2 was increased in sDR5 treatment rats after AMI. DR5 expression was also analysed after sDR5 treatment and it was down-regulated, and a low level of DR5 expression seemed to be beneficial for the myocardium. Overall, our findings indicated that sDR5 decreases myocardial damage by inhibiting apoptosis in rat after AMI. We expect to observe the potential therapeutic effects of sDR5 on AMI in the future.
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Metadaten
Titel
TRAIL inhibition by soluble death receptor 5 protects against acute myocardial infarction in rats
verfasst von
Mingli Wang
Yinxiang Wei
Xuance Wang
Fanni Ma
Weina Zhu
Xi Chen
Xiaoming Zhong
Shulian Li
Jun Zhang
Guangchao Liu
Yaohui Wang
Yuanfang Ma
Publikationsdatum
07.11.2022
Verlag
Springer Japan
Erschienen in
Heart and Vessels / Ausgabe 3/2023
Print ISSN: 0910-8327
Elektronische ISSN: 1615-2573
DOI
https://doi.org/10.1007/s00380-022-02197-7

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