{'fraction_non_alphanumeric': 0.017657992565055763, 'fraction_numerical': 0.007434944237918215, 'mean_word_length': 5.449101796407185, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Diabetes and microvascular pathophysiology: role of epidermal growth factor receptor tyrosine kinase

Type 2 diabetes is responsible for the increased prevalence of ischaemic heart disease, generally related to coronary artery disease, which is associated with increased morbidity and death in diabetic patients. Epidermal growth factor receptor (EGFR) tyrosine kinase, one of the many factors involved in cell growth and migration, has been shown to be key element in the development of microvessel myogenic tone. In a recent study, we have shown that microvascular dysfunction in type 2 diabetes is dependent on the exacerbation of the EGFR tyrosine kinase phosphorylation. Thus, further elucidation of this EGFR transactivation and down stream signalling will offer a new direction to investigate the mechanism of microvascular dysfunction responsible for heart disease that occurs in type 2 diabetes. In this review, we discuss the link between the EGFR transactivation and microvascular dysfunction that occurs in type 2 diabetes. Copyright © 2009 John Wiley & Sons, Ltd.