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Circulation Research. 2004;94:1523
doi: 10.1161/01.RES.0000134760.93885.3a
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(Circulation Research. 2004;94:1523.)
© 2004 American Heart Association, Inc.


Editorials

First Annual Symposium of the American Heart Association Council on Basic Cardiovascular Sciences

Stress Signals, Molecular Targets, and the Genome

Michael D. Schneider

From the Center for Cardiovascular Development, Departments of Medicine, Molecular and Cellular Biology, and Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Tex.

Correspondence to Dr Michael D. Schneider, Center for Cardiovascular Development, Baylor College of Medicine, One Baylor Plaza, Room 506D, Houston, TX 77030. E-mail michaels{at}bcm.tmc.edu


Key Words: stress signals • genomics • molecular targets • basic cardiovascular science

The completed sequence of a human genome, alongside increasingly those of model organisms, in rank of use and tractability, lays before the investigator the raw matter of inherited biology in stark and exquisite reductionist detail. At the dawn of our millennium, this newly arrived state of knowledge—omniscience, with respect to sequence—set into place the concatenation of new questions and bracing opportunities deemed the "postgenomic" era. What genes serve what functions, when, where, and how? (Even the most optimistic among us dispenses with "why?") At a higher level of complexity, what networks of genes serve what functions, and how are these coordinated? How, too, do proteins relate, not just pairwise but in intricate webs of physical associations, counting in the thousands or many tens of thousands? In other words, broad-band biology.

For the cardiovascular sciences, long-separate strands of work converged in recent years, in significant part, because of the shared enabling technologies. Biochemical and biophysical studies of heart-expressed proteins and their genes, including the changes in expression in disease or early heart formation, and the functional changes imparted by mutations, moved increasingly from molecules to cells to gene-modified mice, to engineering other species, and even to rational gene- and cell-based therapies for humans. Conversely, traditional whole-animal studies (the integrative physiology of circulation) responded with equal alacrity to the newly doable: "down-sizing" cath and noninvasive laboratories to take on the mouse, mouse embryo, and transparent zebrafish. From bench to beast, and vice versa.

Five years ago, this convergence resulted in council fusion—the marriage of two historic American Heart Association Councils, Basic Science and Circulation, creating the Council on Basic Cardiovascular Sciences, the Association’s second-most populous council and the world’s premier assemblage of investigators in fundamental cardiovascular research.1 The result is shared problems, tools, and scientific passions. Thanks are due to Leslie Leinwand and Tom Hintze, as the respective Council chairs, for their indispensable leadership and vision in creating the combined Council. From the very start, the resulting synergies have come to bear on postgenomic studies such as functional genomics (linking genes to function, even on a massively parallel, genome-wide scale) and proteomics. During these few years, this process has been catalyzed by several high-visibility initiatives of the National Heart, Lung, and Blood Institute that differ from many other "center" grants in their commitment, as an organizing principle, to develop reagents, databases, and informational tools for use by a broad scientific community.

One means whereby our Council has sought to accelerate not merely the pace of basic discovery, but also the opportunities for translation into testable therapies, has been through periodic symposia. Predictably outstanding in quality, but less predictable in their timing of appearance, these meetings, headed by Seigo Izumo, Bill Balke, Richard Shannon, Mark Taubman, Tish Murphy, Rick Kitsis, and others (too numerous to thank all here), were the successors in both spirit and implementation to the pioneering symposia in Asilomar on the molecular biology of heart disease, crafted long ago by Ken Chien. With time, the membership and leaders have seen the merits of establishing the Council’s meeting on a more permanent, regular, annual footing.

This summer’s symposium (July 14 to 18, 2004, in Stevenson, Washington) marks the first undertaken on this basis and is organized around what is arguably the ur-problem for cardiovascular biology, namely, the genome-wide response to cell stress. As one organizer, I have been indescribably blessed by having three others—Ivor Benjamin, Stefanie Dimmeler, Issei Komuro—of unsurpassable creativity, energy, and discernment. We have been gratified by the mandate provided by the Council to institute an annual summer symposium for cardiovascular research and, in particular, by the efforts by Roberto Bolli and Eduardo Marbán, our current and former Council chairs, to help shepherd this creation at many steps. Through their leadership, for the first time, we are able to offer our participants a permanent and public home for their abstracts, to be found as an online data supplement available at http://circres.ahajournals.org. All of us in the Council leadership, the Council membership, and the conference participants present and future can be especially grateful to the National Heart, Lung, and Blood Institute, which has awarded essential funding to the newly established meeting for the years 2004 through 2008.

Footnotes

The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.

Reference

1. Hintze TH, Marbán E. Two AHA councils become one. Ringing out the old and bringing in the new. Circ Res. 1999; 85: 219–220.[Free Full Text]





This Article
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Right arrow Full Text (PDF)
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Right arrow Alert me when this article is cited
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Right arrow Similar articles in PubMed
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Google Scholar
Right arrow Articles by Schneider, M. D.
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Right arrow Articles by Schneider, M. D.