""Skeletal muscle has the ability to regenerate new muscle fibers after injury. The process of new muscle formation requires that quiescent. mononuclear muscle precursor cells (myoblasts) become activated, proliferate, differentiate, and fuse into multinucleated myotubes which, in. turn, undergo further differentiation and mature to form functional muscle fibers. Previous data demonstrated the crucial role played by. 3-hydroxy 3-methylglutaryl coenzyme A reductase (HMGR), the rate-limiting enzyme of cholesterol biosynthetic pathway, in fetal rat. myoblast (L6) differentiation. This finding, along with epidemiological studies assessing the myotoxic effect of statins, HMGR inhibitors,. allowed us to speculate that HMGR could be strongly involved in skeletal muscle repair. Thus, our research was aimed at evaluating such. involvement: in vitro and in vivo experiments were performed on both mouse adult satellite cell derived myoblasts (SCDM) and mouse. muscles injured with cardiotoxin. Results demonstrate that HMGR inhibition by the statin Simvastatin reduces SCDM fusion index, fast MHC. protein levels by 60% and slow MHC by 40%. Most importantly, HMGR inhibition delays skeletal muscle regeneration in vivo. Thus, besides. complaining of myopathies, patients given Simvastatin could also undergo an impairment in muscle repair.""

Trapani L, Segatto M, La Rosa P, Fanelli F, Moreno S, Marino M, et al. (2012). 3-Hydroxy 3-methylglutaryl Coenzyme A reductase inhibition impairs muscle regeneration. JOURNAL OF CELLULAR BIOCHEMISTRY, 113(6), 2057-2063 [10.1002/jcb.24077].

3-Hydroxy 3-methylglutaryl Coenzyme A reductase inhibition impairs muscle regeneration

SEGATTO, MARCO;MORENO, Sandra;MARINO, Maria;PALLOTTINI, Valentina
2012

Abstract

""Skeletal muscle has the ability to regenerate new muscle fibers after injury. The process of new muscle formation requires that quiescent. mononuclear muscle precursor cells (myoblasts) become activated, proliferate, differentiate, and fuse into multinucleated myotubes which, in. turn, undergo further differentiation and mature to form functional muscle fibers. Previous data demonstrated the crucial role played by. 3-hydroxy 3-methylglutaryl coenzyme A reductase (HMGR), the rate-limiting enzyme of cholesterol biosynthetic pathway, in fetal rat. myoblast (L6) differentiation. This finding, along with epidemiological studies assessing the myotoxic effect of statins, HMGR inhibitors,. allowed us to speculate that HMGR could be strongly involved in skeletal muscle repair. Thus, our research was aimed at evaluating such. involvement: in vitro and in vivo experiments were performed on both mouse adult satellite cell derived myoblasts (SCDM) and mouse. muscles injured with cardiotoxin. Results demonstrate that HMGR inhibition by the statin Simvastatin reduces SCDM fusion index, fast MHC. protein levels by 60% and slow MHC by 40%. Most importantly, HMGR inhibition delays skeletal muscle regeneration in vivo. Thus, besides. complaining of myopathies, patients given Simvastatin could also undergo an impairment in muscle repair.""
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11590/278626
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