Open AccessCell death, dysglycemia and myocardial infarction
Author(s) -
Xiaodong Tian,
Mingxia Cui,
Shiwei Yang,
Yujie Zhou,
Dayi Hu
Publication year - 2013
Publication title -
biomedical reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.607
H-Index - 25
eISSN - 2049-9442
pISSN - 2049-9434
DOI - 10.3892/br.2013.67
Subject(s) - programmed cell death , apoptosis , cell , hypoglycemia , myocardial infarction , medicine , autophagy , necrosis , cell cycle , biology , cancer , insulin , biochemistry , genetics
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.