Abstract:
:Recent evidence has verified the cardioprotective actions of irisin in different diseases models. However, the beneficial action of irisin on hypoxia-reoxygenation (HR) injury under high glucose stress has not been described. Herein our research investigated the influence of irisin on HR-triggered cardiomyocyte death under high glucose stress. HR model was established in vitro under high glucose treatment. The results illuminated that HR injury augmented apoptotic ratio of cardiomyocyte under high glucose stress; this effect could be abolished by irisin via modulating mitochondrial function. Irisin treatment attenuated cellular redox stress, improved cellular ATP biogenetics, sustained mitochondria potential, and impaired mitochondrion-related cell death. At the molecular levels, irisin treatment activated the 5'-adenosine monophosphate-activated protein kinase (AMPK) pathway and the latter protected cardiomyocyte and mitochondria against HR injury under high glucose stress. Altogether, our results indicated a novel role of irisin in HR-treated cardiomyocyte under high glucose stress. Irisin-activated AMPK pathway and the latter sustained cardiomyocyte viability and mitochondrial function.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Fan J,Zhu Q,Wu Z,Ding J,Qin S,Liu H,Miao Pdoi
10.1002/jcp.29030subject
Has Abstractpub_date
2020-02-01 00:00:00pages
1165-1174issue
2eissn
0021-9541issn
1097-4652journal_volume
235pub_type
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