Key result
Dysglycemia may induce myocardial cell death through necrosis, apoptosis, and autophagy, suggesting that modulating cell death could be a promising therapeutic target for myocardial infarction.
Modulating myocardial cell death pathways may be a promising therapeutic target for limiting myocardial infarction injury exacerbated by dysglycemia.
Does not yet support clinical use of cell death modulators in dysglycemic MI; hypothesis-generating for targeted trials.
Dysglycemia (hyper- and hypoglycemia) has been associated with higher mortality among patients suffering from myocardial infarction (MI). Moreover, dysglycemia may induce cell death. Cell death (necrosis, apoptosis and autophagy) is a ubiquitous process that characterizes the course of several diseases, including MI, and occurs in diverse forms varying in mechanism, pattern and consequence. Therefore, cell death is a potential pathway through which dysglycemia affects the outcome of MI and it is essential to regulate myocardial cell death in the treatment of patients with MI caused by dysglycemia. In this review, we summarized the mechanisms of MI at the cellular level and the regulatory effects of dysglycemia on myocardial cell death. The ability to modulate myocardial cell death may be a promising target of new treatments aimed at limiting MI caused by dysglycemia. However, further research is required to elucidate the mechanisms underlying cell death regulation in MI caused by dysglycemia.
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Cui et al. (2013) conducted a review in Myocardial infarction and dysglycemia. Dysglycemia was evaluated. Dysglycemia may induce myocardial cell death through necrosis, apoptosis, and autophagy, suggesting that modulating cell death could be a promising therapeutic target for myocardial infarction.
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