SDF-1 in myocardial repair

Title

SDF-1 in myocardial repair

Creator

Penn M S; Pastore J; Miller T; Aras R

Publisher

Gene Therapy

Date

2012
2012-06

Description

Stem cell therapy for the prevention and treatment of cardiac dysfunction holds significant promise for patients with ischemic heart disease. Excitingly early clinical studies have demonstrated safety and some clinical feasibility, while at the same time studies in the laboratory have investigated mechanisms of action and strategies to optimize the effects of regenerative cardiac therapies. One of the key pathways that has been demonstrated critical in stem cell-based cardiac repair is (stromal cell-derived factor-1) SDF-1:CXCR4. SDF-1:CXCR4 has been shown to affect stem cell homing, cardiac myocyte survival and ventricular remodeling in animal studies of acute myocardial infarction and chronic heart failure. Recently released clinical data suggest that SDF-1 alone is sufficient to induce cardiac repair. Most importantly, studies like those on the SDF-1:CXCR4 axis have suggested mechanisms critical for cardiac regenerative therapies that if clinical investigators continue to ignore will result in poorly designed studies that will continue to yield negative results. Gene Therapy (2012) 19, 583-587; doi:10.1038/gt.2012.32

Subject

acute myocordial infarction; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; chemokines; gene-therapy; Genetics & Heredity; Heart failure; infarction; ischemic cardiomyopathy; mesenchymal stem-cells; pilot trial; regeneration; Regenerative medicine; Research & Experimental Medicine; stem-cells

Identifier

Format

Journal Article

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Rights

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

Pages

583-587

Issue

6

Volume

19

Citation

Penn M S; Pastore J; Miller T; Aras R, “SDF-1 in myocardial repair,” NEOMED Bibliography Database, accessed September 26, 2021, https://neomed.omeka.net/items/show/6752.

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