Inhibition of ALDH2 by O-GlcNAcylation contributes to the hyperglycemic exacerbation of myocardial ischemia/reperfusion injury

Although hyperglycemia is causally related to adverse outcomes after myocardial ischemia/reperfusion (I/R), the underlying mechanisms are largely unknown. Here, we investigated whether excessive O-linked-N-acetylglucosamine (O-GlcNAc) modification of acetaldehyde dehydrogenase 2 (ALDH2), an importan...

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Veröffentlicht in:	Oncotarget 2017-03, Vol.8 (12), p.19413-19426
Hauptverfasser:	Liu, Baoshan, Wang, Jiali, Li, Minghua, Yuan, Qiuhuan, Xue, Mengyang, Xu, Feng, Chen, Yuguo
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylglucosamine - metabolism Aldehyde Dehydrogenase - chemistry Aldehyde Dehydrogenase - metabolism Animals Apoptosis Cell Proliferation Cells, Cultured Glycosylation Humans Hyperglycemia - enzymology Hyperglycemia - etiology Hyperglycemia - pathology Male Myocardial Reperfusion Injury - complications Myocytes, Cardiac - drug effects Myocytes, Cardiac - enzymology Myocytes, Cardiac - pathology Protein Processing, Post-Translational Rats Rats, Wistar Research Paper
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Zusammenfassung:	Although hyperglycemia is causally related to adverse outcomes after myocardial ischemia/reperfusion (I/R), the underlying mechanisms are largely unknown. Here, we investigated whether excessive O-linked-N-acetylglucosamine (O-GlcNAc) modification of acetaldehyde dehydrogenase 2 (ALDH2), an important cardioprotective enzyme, was a mechanism for the hyperglycemic exacerbation of myocardial I/R injury. Both acute hyperglycemia (AHG) and diabetes (DM)-induced chronic hyperglycemia increased cardiac dysfunction, infarct size and apoptosis index compared with normal saline (NS)+I/R rats (P
ISSN:	1949-2553 1949-2553
DOI:	10.18632/oncotarget.14297