Can heart function lost to disease be regenerated by therapeutic targeting of cardiac scar tissue?
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- 作者：Emily L. Ongstada ; ongstad@vt.edu" class="auth_mail" title="E-mail the corresponding author ; Robert G. Gourdiea ; b ; c ; gourdier@vtc.vt.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：αCT1 ; alpha-carboxyl-terminal peptide 1 ; AP ; action potential ; APD ; action potential duration ; BMCs ; bone marrow derived cells ; CV ; conduction velocity ; Cx43 ; connexin 43 ; ECM ; extracellular matrix ; GJ ; gap junction ; GJIC ; gap junction intercellular communication ; IBZ ; injury border zone ; ID ; intercalated disc ; Kir2.1 ; inward rectifying potassium current 2.1 ; KCNH2 ; voltage gated potassium channel ; Kv1.3 ; voltage gated potassium channel 1.3 ; LV ; left ventricular ; MI ; myocardial infarction ; miR-1
- 刊名：Seminars in Cell & Developmental Biology
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：58
- 期：Complete
- 页码：41-54
- 全文大小：1489 K
文摘
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The adult heart cannot regenerate, so myocardial infarction (MI) results in a scar.
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Significant electrical and mechanical remodeling occurs after MI, resulting in arrhythmias.
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Modifying scar properties is a viable strategy for improving post-MI prognosis.
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Proteins involved in conduction and fibrous tissue structure are primary targets for altering scar properties.
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Further study is required to understand how modifying scar tissue affects heart function.