Early citalopram treatment increases mortality due to left ventricular rupture in mice after myocardial infarction
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- 作者：Anna Freya ; c ; frey_a@ukw.de" class="auth_mail" title="E-mail the corresponding author ; Veronica-Maria Saxona ; c ; Sandy Poppb ; c ; Marc Lehmanna ; c ; Denise Mathesc ; Christina Pachelc ; Ulrich Hofmannd ; Georg Ertla ; c ; Klaus-Peter Leschb ; c ; 1 ; Stefan Frantzd ; 1
- 关键词：MI ; myocardial infarction ; SSRI ; selective serotonin reuptake inhibitor ; LPS ; lipopolysaccharide ; IL ; interleukin ; MMP ; matrix metalloproteinase ; TIMP ; tissue inhibitor of metalloproteinase ; CIT ; citalopram ; LAD ; left anterior descending coronary artery ; SAL ; saline 0 ; 9% ; DMSO ; dimethyl sulfoxide) ; α-SMA ; alpha smooth muscle actin ; TGF β ; transforming growth factor beta ; TNF α ; tumor necrosis factor alpha ; SERT ; serotonin transporter ; 5HT2A ; serotonin receptor 2a ; 5HT2B ; serotonin receptor 2b ; P
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：98
- 期：Complete
- 页码：28-36
- 全文大小：1367 K
文摘
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Citalopram treatment causes increased mortality after myocardial infarction in mice.
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Ventricular rupture due to MMP-13 upregulation is the responsible mechanism.
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MMP inhibition with PD166793 can partially reverse the effects of citalopram.
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Caution is called for start of citalopram in humans after myocardial infarction.