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Non-Pharmacological Interventions in Refractory Angina 难治性心绞痛的非药物干预
Pub Date : 2018-12-30 DOI: 10.17140/HROJ-5-146
N. Ali, P. Patel
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引用次数: 3
Inhibiting the Inhibitors, PTP1B as a Therapeutic Target in Myocardial Infarction 抑制PTP1B抑制剂作为心肌梗死的治疗靶点
Pub Date : 2018-12-30 DOI: 10.17140/HROJ-5-147
L. Fiedler
Mini-Review | Volume 5 | Number 1| 8 Copyright 2018 by Fiedler LR. This is an open-access article distributed under Creative Commons Attribution 4.0 International License (CC BY 4.0), which allows to copy, redistribute, remix, transform, and reproduce in any medium or format, even commercially, provided the original work is properly cited. cc Biological systems self-regulate through cycles of activation and inactivation, the balance of which is critical in permitting or suppressing signaling cascades and their downstream consequences. Kinase signaling pathways are regulated through phosphorylation (activation) and dephosphorylation (inactivation) events. Hyperactivity of kinase pathways plays a causal and critical role in the development of cardiac pathologies, and as such, the development of pharmacological inhibitors has been an intense area of investigation. Conversely, enhancing the activity of suppressed, but potentially beneficial kinase activities present an alternative therapeutic avenue. In this context, kinase dephosphorylation by phosphatases results in inactivation and suppression of the pathway. Thus inhibiting the inhibitors provides a method by which to enhance the activity of selected pathways. The protein tyrosine phosphatase 1B (PTP1B) has been implicated as a therapeutic target in several diseases but was considered to be undruggable. More recent development of inhibitors with improved specificity and pharmacological properties along with identification of novel indications has sparked renewed interest. This mini-review summarises the current status of PTP1B inhibitors in clinical trials and in pre-clinical models for new indications; myocardial infarction and heart failure.
迷你评论|第五卷|第1期|第8期版权所有:Fiedler LR。这是一篇在知识共享署名4.0国际许可(CC BY 4.0)下发布的开放获取文章,允许在任何媒介或格式下复制、再分发、再混合、转换和复制,甚至是商业复制,只要正确引用原始作品。生物系统通过激活和失活的循环进行自我调节,其平衡对于允许或抑制信号级联及其下游后果至关重要。激酶信号通路是通过磷酸化(激活)和去磷酸化(失活)事件调节的。激酶通路的过度活跃在心脏病理的发展中起着因果和关键作用,因此,药物抑制剂的开发一直是一个激烈的研究领域。相反,增强抑制但潜在有益的激酶活性提供了另一种治疗途径。在这种情况下,磷酸酶的激酶去磷酸化导致该途径的失活和抑制。因此,抑制抑制剂提供了一种增强所选途径活性的方法。蛋白酪氨酸磷酸酶1B (PTP1B)已被认为是几种疾病的治疗靶点,但被认为是不可药物的。最近开发的抑制剂具有更好的特异性和药理学性质,以及识别新的适应症,引发了新的兴趣。这篇小型综述总结了PTP1B抑制剂在临床试验和新适应症临床前模型中的现状;心肌梗塞和心力衰竭。
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引用次数: 3
Three-Dimensional Printing-Generated Realistic Anatomy Models and Virtual Endoscopy-Enhanced Intravascular Assessment of Pathologies 三维打印生成的真实解剖模型和虚拟内窥镜-增强病理血管内评估
Pub Date : 2018-12-30 DOI: 10.17140/HROJ-5-E009
Zhonghua Sun, Sultan Aldosari
Editorial | Volume 5 | Number 1| e1 Copyright 2018 by Sun Z. This is an open-access article distributed under Creative Commons Attribution 4.0 International License (CC BY 4.0), which allows to copy, redistribute, remix, transform, and reproduce in any medium or format, even commercially, provided the original work is properly cited. cc T (3D) printing has become a widely used technique showing many medical applications which range from orthopedics and maxillofacial surgery to cardiovascular disease and tumor imaging.1-10 Computed tomography (CT) or magnetic resonance imaging (MRI) data-generated 3D printed realistic models have been confirmed to accurately replicate normal anatomical structures and depict pathological changes including a demonstration of complex pathologies such as complicated cardiovascular disease.7-11 3D printed models also serve as a useful tool for pre-surgical planning, simulation of surgical procedures, training medical students and young doctors, and enhancing patient-doctor communications.12-16
编辑| Volume 5 | Number 1| e1 Copyright 2018 by Sun Z.这是一篇基于知识共享署名4.0国际许可(CC by 4.0)的开放获取文章,允许以任何媒介或格式复制、再分发、再混合、转换和复制,即使是商业复制,前提是正确引用原始作品。从骨科、颌面外科到心血管疾病和肿瘤成像,3D打印已经成为一种广泛使用的医学技术。1-10计算机断层扫描(CT)或磁共振成像(MRI)数据生成的3D打印逼真模型已被证实能够准确复制正常解剖结构并描绘病理变化,包括复杂病理的演示,如复杂的心血管疾病。7-11 3D打印模型还可作为术前规划、外科手术过程模拟、培训医学生和年轻医生以及加强医患沟通的有用工具
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引用次数: 1
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Heart Research - Open Journal
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