Detailed Instructions: In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
Problem:Context: -Enolase is a glycolytic enzyme with "second jobs" beyond its catalytic activity. However, its possible contribution to cardiac dysfunction remains to be determined. The present study aimed to investigate the role of -enolase in doxorubicin (Dox)-induced cardiomyopathy as well as the underlying mechanisms.', 'The expression of -enolase was detected in rat hearts and primary cultured rat cardiomyocytes with or without Dox administration. An adenovirus carrying short-hairpin interfering RNA targeting -enolase was constructed and transduced specifically into the heart by intramyocardial injection. Heart function, cell apoptosis and mitochondrial function were measured following Dox administration. In addition, by using gain- and loss-of-function approaches to regulate -enolase expression in primary cultured rat cardiomyocytes, we investigated the role of endogenous, wide type and catalytically inactive mutant -enolase in cardiomyocyte apoptosis and ATP generation. Furthermore, the involvement of -enolase in AMPK phosphorylation was also studied.', 'The mRNA and protein expression of cardiac -enolase was significantly upregulated by Dox. Genetic silencing of -enolase in rat hearts and cultured cardiomyocytes attenuated Dox-induced apoptosis and mitochondrial dysfunction. In contrast, overexpression of wide-type or catalytically inactive -enolase in cardiomyocytes mimicked the detrimental role of Dox in inducing apoptosis and ATP reduction. AMPK dephosphorylation was further demonstrated to be involved in the proapoptotic and ATP-depriving effects of -enolase.\Question: Does -Enolase play a catalytically independent role in doxorubicin-induced cardiomyocyte apoptosis and mitochondrial dysfunction?
Solution:
Our findings provided the evidence that -enolase has a catalytically independent role in inducing cardiomyocyte apoptosis and mitochondrial dysfunction, which could be at least partially contributed to the inhibition of AMPK phosphorylation.