Role of the SDF-1-CXCR4 axis in stem cell-based therapies for ischemic cardiomyopathy

被引：124

作者：

Zaruba, Marc-Michael ^{[1
,2
]}

Franz, Wolfgang-Michael ^{[1
]}

机构：

[1] Univ Munich, Klinikum Grosshadern, Dept Med 1, D-81377 Munich, Germany

[2] Indiana Univ, Sch Med, Riley Heart Res Ctr, Indianapolis, IN 46202 USA

来源：

EXPERT OPINION ON BIOLOGICAL THERAPY | 2010年 / 10卷 / 03期

关键词：

CXCR4; homing; ischemic cardiomyopathy; SDF-1; ACUTE MYOCARDIAL-INFARCTION; COLONY-STIMULATING FACTOR; ENDOTHELIAL PROGENITOR CELLS; LEFT-VENTRICULAR FUNCTION; COMBINED IMMUNODEFICIENCY MICE; RANDOMIZED CONTROLLED-TRIALS; CHEMOKINE RECEPTOR CXCR4; BONE-MARROW-CELLS; HEMATOPOIETIC STEM; FACTOR-I;

D O I：

10.1517/14712590903460286

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Importance of the field. Ischemic disorders are the leading cause of mortality worldwide, current therapies only delay progression of the disease. Data suggest a role of the SDF-1-CXCR4 axis in attenuation of ischemic disorders. Areas covered in this review: We discuss the importance of SDF-1-CXCR4 interactions during development and postnatal mobilization and migration of stem cells. We focus on the role of the SDF-1-CXCR4 axis in stem-cell-based applications for attenuation of ischemic cardiomyopathy. What the reader will gain: During development the SDF-1-CXCR4 axis plays a critical role in gradient-guided cell movements. In adults, the SDF-1-CXCR4 axis is involved in retention and mobilization of stem cells. Since SDF-1 is upregulated during hypoxic tissue damage, strategies to augment or stabilize SDF-1 have been utilized to target blood-derived stem cells to ischemic tissue. We exploited this concept by preventing SDF-1 degradation with dipeptidylpeptidaseIV (DPPIV) inhibition and mobilization of stem cells by G-CSF after acute myocardial infarction. This targeted CD34(+)CXCR4(+) cells to ischemic heart and attenuated ischemic cardiomyopathy. Take home message: The SDF-1-CXCR4 axis plays a role in stem cell homing during embryogenesis and adulthood especially after ischemia. Preserving functional SDF-1 by DPPIV inhibition after ischemia may enhance stem cell therapies.

引用

页码：321 / 335

页数：15

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