title: Tear me down: role of calpain in the development of cardiac ventricular hypertrophy.
abstract: Cardiac hypertrophy develops most commonly in response to hypertension and is an independent risk factor for the development of heart failure. The mechanisms by which cardiac hypertrophy may be reversed to reduce this risk have not been fully determined to the point where mechanism-specific therapies have been developed. Recently, proteases in the calpain family have been implicated in the regulation of the development of cardiac hypertrophy in preclinical animal models. In this review, we summarize the molecular mechanisms by which calpain inhibition has been shown to modulate the development of cardiac (specifically ventricular) hypertrophy. The context within which calpain inhibition might be developed for therapeutic intervention of cardiac hypertrophy is then discussed.
authors.affiliation: McAllister Heart Institute, University of North Carolina at Chapel Hill, 27599-7525, USA.
authors.forename: Cam
authors.initials: C
authors.lastname: Patterson
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Portbury
authors.forename: Jonathan C
authors.initials: JC
authors.lastname: Schisler
authors.forename: Monte S
authors.initials: MS
authors.lastname: Willis
mesh_terms: D000818:Animals; D002154:Calpain / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006332:Cardiomegaly / Q000201:enzymology* / Q000473:pathology / Q000517:prevention & control; D002317:Cardiovascular Agents / Q000494:pharmacology; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D015195:Drug Design; D006352:Heart Ventricles / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D006801:Humans; D015398:Signal Transduction / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents; D015853:Cysteine Proteinase Inhibitors; D002154:Calpain