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(Circulation Research. 2007;100:1537.)
© 2007 American Heart Association, Inc.

Editorials

Resizing the Genomic Regulation of Restenosis

Takumi Matsumoto, Paul M. Hwang

From the Cardiology Branch, NHLBI, National Institutes of Health, Bethesda, Md.

Correspondence to Paul M. Hwang, MD, PhD, Cardiology Branch, National Institutes of Health, Bldg. 10-CRC, Rm. 5-5330, 10 Center Drive, Bethesda, MD 20892-1454. E-mail hwangp@mail.nih.gov

See related article, pages 1579–1588

Key Words: microRNA • vascular smooth muscle cells • neointima • cell cycle

An extract of the first 250 words of the full text is provided, because this article has no abstract.

With the introduction of drug eluting stents (DES) for percutaneous coronary interventions, restenosis appeared to be a problem of the past. However, the biology of arterial injury has returned to the limelight of clinical cardiology because of increased late-stent thrombosis associated with DES.¹ As DES use initially increased, concerns were raised about altering the normal responses to arterial injury with antiproliferative drugs based on animal and human data.² Since 2006, this concern has translated to dramatic decreases in DES deployment in catherization laboratories across the U.S. These events serve to underscore the importance of continuing to incorporate new clinical and basic experimental data for improving patient management.

In a different realm, developmental biologists working on the primitive earthworm Caenorhabditis elegans discovered a novel regulatory mechanism involving short pieces of RNA (microRNA or miRNA) for which they were awarded the 2006 Nobel Prize in Physiology/Medicine. Over 500 different miRNAs have now been identified in the mouse and human genomes (miRBase: http://microrna.sanger.ac.uk/); a schematic overview of miRNA biogenesis is provided in the Figure (A). miRNAs generally act on their target messenger RNAs (mRNA) by promoting RNA degradation or inhibiting protein translation. They are expressed in a tissue- and condition-specific manner indicating their potential role in normal development and disease pathogenesis.³ They appear to regulate diverse processes such as cell proliferation, cell death, metabolism, hematopoiesis, angiogenesis, and tumorigenesis.^3–6 Emerging genetic evidence also suggests an essential role of miRNAs in normal cardiogenesis and abnormal stress responses such as hypertrophy and arrhythmogenesis.^7–9 There are also . . . [Full Text of this Article]