Cardiovascular Injury and Repair Research Facility

描述（由申请人提供）： 在过去的25年里，生理学和内科（心脏病学分部）在弗吉尼亚联邦大学（VCD）的部门一直保持着心血管损伤和修复的高产研究计划。一个由杰出的研究人员组成的核心小组每年进行超过250万美元的NIH资助的研究;与这个团队合作的教师进行额外的220万美元。该提案要求提供资金，用于翻新桑格大厅三楼的13，842平方英尺，用于心血管损伤和修复研究设施。拟议的设施将作为一个磁铁，招募研究人员的生理学系，其中有4个开口;研究副总裁已承诺高达160万美元的启动包提供。核心研究团队将开发在细胞、遗传和分子水平上有效修复受损和患病心脏组织的创新方法。他们试图了解内源性因子如何保护和修复心脏，以及如何用工程替代品成功地替换受损组织。具体而言，它们将：  确定触发心脏保护预处理的分子和遗传机制;  开发成体心脏干细胞治疗方法以治疗心血管损伤;  确定决定横纹肌氧交换几何和血液动力学因素;  开发用于重建功能障碍或缺失的心脏组织的横纹肌假体;  确定正常心脏中离子通道功能的分子机制，通过 病理条件和患病心脏中药理学试剂的离子通道调节。

DESCRIPTION (provided by applicant): Over the past 25 years, the Departments of Physiology and Internal Medicine (Division of Cardiology) at Virginia Commonwealth University (VCD) have maintained a highly productive research program in cardiovascular injury and repair. An established core group of outstanding investigators conduct more than $2.5 million annually of NIH-funded research; faculty collaborating with this team conduct an additional $2.2 million. This proposal requests funds to renovate 13,842 sq ft on the 3rd floor of Sanger Hall for the Cardiovascular Injury and Repair Research Facility. The proposed facility will serve as a magnet to recruit research faculty to the Department of Physiology, which has 4 openings; the Vice President for Research has committed up to $1.6 million toward the start-up packages to be offered. The core research team will develop innovative methods of effectively repairing damaged and diseased cardiac tissue at a cellular, genetic, and molecular level. They seek to learn how endogenous factors can protect and repair the heart and how damaged tissue can be successfully replaced with engineered substitutes. Specifically, they will:  identify molecular and genetic mechanisms for triggering cardioprotective preconditioning;  develop adult cardiac stem cell therapeutic approaches to treating cardiovascular injury;  identify geometric and hemodynamic factors that determine oxygen exchange in striated muscle;  develop a striated muscle prosthesis for the reconstruction of dysfunctional or missing cardiac tissue;  identify molecular mechanisms for ion channel function in normal heart, ion channel remodeling by pathological conditions, and ion channel modulation by pharmacological agents in diseased heart.