Copyright © 2005, European Society of Cardiology
The ubiquitin–proteasome system may be involved in the pathogenesis of hypertrophic cardiomyopathy
Max-Planck-Institute of Heart and Lung Research, Experimental Cardiology Benekestr. 2, D-61231 Bad Nauheim Germany
* Private address: Richard-Kuhn-Str. 43 D-69123 Heidelberg, Germany. Email address: hanspeter_vosberg@web.de
Received 1 February 2005; accepted 1 February 2005
| The first 150 words of the full text of this article appear below. |
See also article by Sarikas et al. [7] (pages 33–44) in this issue.
Cardiac morbidity results in the majority of cases from conditions that do not arise in the myocardium itself, but rather in response to extra-myocardial challenges associated with systemic, vascular, or other dysfunctions. A few, not particularly frequent cardiac disorders, however, can be traced to an impairment from within the myocardium. Many, if not most, of these conditions have a genetic cause. Mutations in numerous genes have been identified, most notably in genes coding for proteins involved in contraction and force development, electrical conductance, and in structure and maintenance of the cyto- and nucleoskeleton.
Particularly well studied among the genuinely myocardial disorders have been the cardiomyopathies, clinically well known for decades and characterized by distorted force production affecting either diastole (relaxation) or systole (contraction). Impaired diastole and systole are hallmarks of hypertrophic- (HCM) and dilated cardiomyopathy (DCM),
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  O. Tsukamoto, T. Minamino, and M. Kitakaze Functional alterations of cardiac proteasomes under physiological and pathological conditions Cardiovasc Res, September 4, 2009; (2009) cvp282v2. [Abstract] [Full Text] [PDF]
|
|