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(Circulation Research. 2007;101:114.)
© 2007 American Heart Association, Inc.

Editorials

Translational Medicine With a Capital T, Troponin T, That Is

R. John Solaro

From the Department of Physiology and Biophysics, and Center for Cardiovascular Research, College of Medicine, University of Illinois at Chicago.

Correspondence to R. John Solaro, PhD, Department of Physiology and Biophysics, University of Illinois at Chicago, 835 S. Wolcott Ave (M/C 901), Chicago, IL 60612. E-mail solarorj@uic.edu

See related article, pages 185–194

Key Words: sarcomere • thin filaments • dilated cardiomyopathy • phosphorylation

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

	Introduction

 
Although the quest to translate understanding at the molecular level to the prevention, diagnosis, and therapy of disorders of the heart has been ongoing in many laboratories for many years, the recently popular term "translational medicine" is useful to convey the reality of this objective to our leaders in government, industry, and the academy. In my judgment there is no better example of translational medicine than the identification of sarcomeric mutations linked to cardiomyopathies and sudden death. These myopathies identified by linkage analysis were the first cardiac conditions to be understood at the molecular level of organization.¹ "Translation" requires determination of the primary effect of the mutation on function at the level of the cardiac sarcomeres and the cells, and integration of these findings at the level of the organ and the organism. This knowledge sets the stage for rational diagnosis, prevention, and therapy.

An extensive analysis of this sort in a mouse model has been performed by Du et al² and is reported in the present issue. The focus of their work was on troponin T (TnT), a thin filament protein, which, together with troponin-I, troponin-C, and tropomyosin, imposes Ca²⁺-regulation on the actin-myosin reaction.³ Du et al generated a knock-in mouse model of a deletion mutant of TnT, TNNT2^K210/K210, which had been linked to DCM.¹ TnT-K210 is localized in a critical region of TnT that has multiple interactions with its neighbors on the thin filament and is critical for regulation by Ca²⁺.³ The transgenic mice demonstrated . . . [Full Text of this Article]

Related Article:

Knock-In Mouse Model of Dilated Cardiomyopathy Caused by Troponin Mutation

Cheng-Kun Du, Sachio Morimoto, Kiyomasa Nishii, Reiko Minakami, Mika Ohta, Naoto Tadano, Qun-Wei Lu, Yuan-Yuan Wang, Dong-Yun Zhan, Misato Mochizuki, Satomi Kita, Yoshikazu Miwa, Fumi Takahashi-Yanaga, Takahiro Iwamoto, Iwao Ohtsuki, and Toshiyuki Sasaguri
Circ. Res. 2007 101: 185-194. [Abstract] [Full Text] [PDF]