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[TCT2008]细胞和分子心肌修复的争论

发布于:2008-10-16 19:31    


韩玮,医学博士,心内科主治医师,发表论文10余篇,主要从事心血管疾病介入治疗

Hanwei, attending physician in Cardiology department of the General Hospital of Chinese Armed Police Forces, doctor degree in PLA General Hospital. Be proficiency in transradial coronary artery disease interventional therapy, IVUS and Multi-slice computed tomography coronary artery imagination, published 14 articles and 3 books recent years.

 

细胞和分子心肌修复的争论

 

Up for Debate: Cells vs. Molecules for Repair of Cardiac Tissue

 

(北京武警总医院 韩玮 翻译)


关于未来心肌细胞治疗的专题讨论中四个专家就全细胞或小分子或蛋白哪个是恢复受损心肌组织功能的最佳策略展开了辩论。

 

新组织

 

德国法兰克福大学的Stefanie Dimmeler和New Haven 大学医学院的Frank J. Giordano讨论了蛋白和小分子在心肌组织修复中的作用。Dimmeler使用瘢痕组织标本来评价多种细胞治疗因子的治疗作用。他说,“瘢痕组织是死的,需要提供一些活的东西,我们仅注射生长因子到瘢痕组织里面不会解决终末期心衰的问题,需要导入新的组织,细胞才有可能存活。”


Giordano质疑类肌肉组织的分化是否能带来心肌功能上的改变,例如心脏大约有26亿肌细胞和两倍于该数字的其他类型细胞,如果注射1千万个细胞且全部存活,也仅是全部细胞数量的一小部分。这似乎不太可能引起心脏功能的改变,更可行的方法是寻找一个输送系统或基质来捕获或注射到希望到达的部位。

 

伦敦的Jonathan M. Hill教授支持用全细胞来修复心肌,我们可以获得复杂的细胞生物学效应说法是一种倒退,一种方法或一个分子是不可能有这种复杂作用的,我们要思索系统的生物学效应,是否这些细胞能释放小分子蛋白并不清楚。

 

Indiana血管生物学中心的Keith L March说争论没有什么必要,“这两个观点都不可取,重要的是要明确细胞移植后发生了什么,就象REPAIR-MI 试验,一类细胞也可能不足够。”

 

(来源:www.tctmd.com

 


Up for Debate: Cells vs. Molecules for Repair of Cardiac Tissue 


Key Points:


In end-stage HF, function will not be restored if growth factors are simply injected into scar tissue.

 

By TCT Daily Staff

 

In a session held Monday about the future of cardiac cell therapy, four experts considered whether whole cells or small molecules and proteins represent the best strategy for restoring function to damaged cardiac tissue.

 

New tissue needed

 

Stefanie Dimmeler, PhD, from the University of Frankfurt, Germany, and Frank J. Giordano, MD, of Yale University School of Medicine, in New Haven, Conn., discussed the role of proteins and small molecules in cardiac tissue repair. Dimmeler focused on the example of scar tissue in assessing the therapeutic value of different factors for cell therapy.

 

"Scar tissue is dead, and you need to provide something living [to repair it]. We will not solve the problem of end-stage heart failure if we just inject growth factors into scar tissue," he said. "You need something to introduce new tissue, and for this, cells might be a good way."

 

Giordano, though, questioned whether "you can really make any kind of functional change in the heart based on myocyte differentiation."

 

For example, there are roughly 2.6 billion muscle cells and twice that number of other cell types in the heart. If 10 million cells are injected and if all of them survive, that would represent only a tiny change in the total number of cells, Giordano said.

 

"To think that is going to change heart function is a bit of a reach. What is more viable is [to create] a delivery system or a matrix to capture and inject what it is you want to deliver," he said.

 

More than the sum of its parts

 

Jonathan M. Hill, MB, ChB, of King’s College Hospital in London, argued in favor of the primacy of cells for cardiac tissue repair. "It’s a retrograde, reductionist step to say we can achieve this complex effect of the biology of the cell, which cannot be replicated by one pathway or one molecule," he said. "We have to think in terms of the biology of systems. Cells are here to stay, but whether they are cells to deliver small molecules and proteins, I don’t know."

 

Keith L. March, MD, PhD, of the Indiana Center for Vascular Biology and Medicine in Indianapolis, suggested there is little to debate. "Both views are reductionist. It is important to build upon what is happening now with cells, as in the REPAIR-MI trial," he said. "It is also probably true that one cell [type] is not enough. The fact is everything that’s been said here is compatible."

 

Disclosures:

Drs. Dimmeler, Giordano, Hill, and March report no relevant conflicts of interest.


 (source:www.tctmd.com

 

 



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