S100A4 protects the myocardium against ischemic stress

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• 作者：Shirin Doroudgar ; PhD^a ; ^b ; ^c ; Pearl Quijada ; PhD^a ; Mathias Konstandin ; MD^a ; ^b ; ^c ; Kelli Ilves ; BS^a ; Kathleen Broughton ; PhD^a ; Farid G. Khalafalla ; PhD^a ; Alexandria Casillas^a ; Kristine Nguyen^a ; Natalie Gude ; PhD^a ; Haruhiro Toko ; MD^a ; Luis Ornelas ; BS^a ; Donna J. Thuerauf ; MS^a ; Christopher C. Glembotski ; PhD^a ; Mark A. Sussman ; PhD^a ; Mirko Vö ; lkers ; MD^a ; ^b ; ^c ; ^{Mirko.voelkers@med.uni-heidelberg.de}
• 关键词：S100A4 ; Myocardial infarction ; Remodeling
• 刊名：Journal of Molecular and Cellular Cardiology
• 出版年：2016
• 出版时间：November 2016
• 年：2016
• 卷：100
• 期：Complete
• 页码：54-63
• 全文大小：1774 K
• 卷排序：100

文摘

Deletion of S100A4 results in decreased cardiac function after myocardial infarction. S100A4 Overexpression protects the myocardium against cell death. S100A4 Overexpression improves cardiac function after myocardial infarction. Correctly-timed S100A4 therapy could be a potent combinatorial approach to prevent degenerative changes after ischemic damage.