Cardiac Progenitor Cell-Derived Extracellular Vesicles: a Rising Star for Cardiac Repair and Regeneration
Cardiac Progenitor Cell-Derived Extracellular Vesicles: a Rising Star for Cardiac Repair and Regeneration
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心脏祖细胞来源的细胞外囊泡：心脏修复和再生的后起之秀
DOI：
10.1007/s12265-018-9862-5
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发表时间：
2019
影响因子：
3.4
通讯作者：
Yihua Bei
中科院分区：
文献类型：
--
作者：
Zhongrong Zhang;Yi Duan;Yihua Bei
心血管疾病是全球死亡和残疾的重要原因[1]。心肌梗塞（MI），在其他心血管疾病中，引起大量心肌细胞损失和代替死亡心肌组织的瘢痕形成，从而导致不利的心脏重塑和心力衰竭。目前对心脏缺血性损伤的治疗主要集中在限制心肌细胞死亡和抑制组织损伤引起的纤维化反应，但不能实现丢失的心脏组织的恢复。因此，在许多心脏病发作的情况下，即使有适当的治疗，梗死也会导致严重的心脏重塑，心输出量下降，最终导致心力衰竭。真正的细胞替代和心肌修复一直是心肌梗死治疗的最终目标，外源性干细胞移植是挽救功能心肌的一种方法。已经在动物模型中测试了各种来源的干细胞候选物，其中心脏来源的祖细胞具有特别的潜力[2，3];然而，尽管有良好的临床前结果，但干细胞治疗中外源性细胞的长期存活率较差，导致其有益效果背后的机制存在争议。事实上，大多数（如果不是全部的话）移植的细胞不能在体内分化为心肌细胞。因此，旁分泌
Cardiovascular diseases represent a significant cause of death and disability worldwide [1]. Myocardial infarction (MI), among other cardiovascular diseases, causes massive cardiomyocyte loss and scar formation in place of dead myocardial tissues, thus leading to adverse cardiac remodeling and heart failure. Current treatments for cardiac ischemic injury mainly focus on limiting the cardiomyocyte death and suppressing the fibrogenic response caused by tissue damage, but cannot achieve a restoration of lost cardiac tissues. Therefore in many cases of heart attack, even with proper treatments, the infarction will cause severe cardiac remodeling, cardiac output decline, and eventually heart failure. True cellular replacement and myocardial restoration is always the ultimate goal of the treatment for MI.One approach for salvage of functional myocardium is transplantation of exogenous stem cells. Various sources of stem cell candidates have been tested in animal models, among which heart-derived progenitor cells hold particular potential [2, 3]; however, the poor long-term survival of the exogenous cells in stem cell therapy causes controversy in mechanism behind the beneficial effects despite the promising preclinical outcomes. Actually, the majority, if not all, of the transplanted cells are not able to differentiate to cardiomyocytes in vivo. Consequently, the paracrine