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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:804.)
© 2004 American Heart Association, Inc.

Editorials

Control of Smooth Muscle Cell Activation

Giulio Gabbiani

From the Department of Pathology, University of Geneva Medical Faculty, Geneva, Switzerland; and the Texas Heart Institute, Houston, Texas.

Correspondence to Giulio Gabbiani, Department of Pathology, University of Geneva Medical Faculty, CMU, 1 rue Michel Servet, 1211Geneva 4, Switzerland. E-mail giulio.gabbiani@medecine.unige.ch

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

We have learned from Thomas Kuhn that during periods of "ordinary" science, observations and facts accumulate, conferring upon a given problem an increasing degree of complexity, up to the moment that a scientific revolution opens a new horizon and brings back more simplicity.¹ Before these revolutions take place, scientists strongly experience the need for placing some order in a field that becomes more and more complicated. A certain proportion of the "ordinary" scientists feel irritated by their colleagues who contribute to the accumulation of new facts thus increasing complexity, which in some instances they call "confusion."

See page 845

During the last several years, biological and medical researchers as well as the general public have lived with the paradigm, still very popular today, that understanding the genetic basis of a given disease represents the key to understanding its biological mechanisms and to developing efficient therapeutic strategies. While this assumption remains basically true, more and more observations have accumulated in favor of the possibility that epigenetic events play an additional and crucial role in the development and evolution of many pathological situations. This applies particularly to a disease such as atheromatosis that has for a long time been considered to be pluricausal.

In the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Braun-Dullaeus et al,² based on previous work of their laboratory and of other laboratories,^3,4 have investigated a particular aspect of arterial smooth muscle cell (SMC) activation, ie, the hypothesis that the susceptibility of SMC to cytokine stimulation depends . . . [Full Text of this Article]