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Trapani, L., Melli, L., Segatto, M., Trezza, V., Campolongo, P., Jozwiak, A., Swiezewska, E., Pucillo, L.P., Moreno, S., Fanelli, F., Linari, M. and Pallottini, V. (2011) Effects of myosin heavy chain (MHC) plasticity induced by HMGCoA-reductase inhibition on skeletal muscle functions. FASEB Journal, 25, 4037-4047. doi:10.1096/fj.11-184218

has been cited by the following article:

• TITLE: HMG CoA reductase inhibition by Simvastatin gets rat β-Myosin heavy chain disappeared: A statin paradox

  AUTHORS: Laura Trapani, Marco Segatto, Adam Jozwiak, Ewa Swiezewska, Valentina Pallottini

  KEYWORDS: Heart; Myosin Heavy Chains; Statins; Ubiquinone

  JOURNAL NAME: Open Journal of Molecular and Integrative Physiology, Vol.3 No.1, February 18, 2013

  ABSTRACT: 3-hydroxy-3methylglutaryl Coenzyme A reductase, the rate limiting enzyme of mevalonate pathway, generates, in addition to cholesterol, a range of products involved in several biological functions: oligoprenyl groups, dolichol and ubiquinone. The latter, in particular, participates in electron transport chain and, in turn, in tissue energy supply. The enzyme is inhibited by statins that, besides lowering cholesterolemia, seem to impair human energy-dependent myocardial functions (e.g. stroke volume, cardiac output, and contractile index). The modulation of heart contractile properties could be explained by the decrease of ventricle ubiquinone content and/or by putative changes in proportion of the different myosin heavy chain isoforms. Since we previously demonstrated that chronic statin treatment modifies myosin heavy chain isoform pattern in skeletal muscle impairing its functional properties, this work was aimed at investigating the effects of statin chronic treatment on both ventricle ubiquinone content and myosin heavy chain isoforms. Our results showed that simvastatin treatment leads to a reduced amount of rat ventricle ubiquinone and to β myosin heavy chain disappearance. Thus, statins which are prescribed to prevent cardiovascular disease, might induce cardiac metabolic and structural modifications whose functional implications on contractility are still to be established and carefully considered.