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  • Altun M, Besche HC, Overkleeft HS, Piccirillo R, Edelmann MJ, Kessler BM, Goldberg AL, Ulfhake B (2010) Muscle wasting in aged, sarcopenic rats is associated with enhanced activity of the ubiquitin proteasome pathway. J. Biol. Chem. 285, 3959739608.
  • Communal C, Sumandea M, de Tombe P, Narula J, Solaro RJ, Hajjar RJ (2002) Functional consequences of caspase activation in cardiac myocytes. Proc. Natl. Acad. Sci. U.S.A. 99, 62526256.
  • Costelli P, Tullio RD, Baccino FM, Melloni E (2001) Activation of Ca(2 + )-dependent proteolysis in skeletal muscle and heart in cancer cachexia. Br. J. Cancer 84, 946950.
  • D'Angelo MG, Gandossini S, Martinelli Boneschi F, Sciorati C, Bonato S, Brighina E, Comi GP, Turconi AC, Magri F, Stefanoni G, Brunelli S, Bresolin N, Cattaneo D, Clementi E (2012) Nitric oxide donor and non steroidal anti inflammatory drugs as a therapy for muscular dystrophies: evidence from a safety study with pilot efficacy measures in adult dystrophic patients. Pharmacol. Res. 65, 472479.
  • Dargelos E, Brulé C, Combaret L, Hadj-Sassi A, Dulong S, Poussard S, Cottin P (2007) Involvement of the calcium-dependent proteolytic system in skeletal muscle aging. Exp. Gerontol. 42, 10881098.
  • Dayton WR, Reville WJ, Goll DE, Stromer MH (1976) A Ca2+-activated protease possibly involved in myofibrillar protein turnover. Partial characterization of the purified enzyme. Biochem. 15, 21592167.
  • Du J, Wang X, Miereles C, Bailey JL, Debigare R, Zheng B, Price SR, Mitch WE (2004) Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions. J. Clin. Invest. 113, 115123.
  • Evans W (1997) Functional and metabolic consequences of sarcopenia. J. Nutr. 127, 998S1003S.
  • Ferrington DA, Krainev AG, Bigelow DJ (1998) Altered turnover of calcium regulatory proteins of the sarcoplasmic reticulum in aged skeletal muscle. J. Biol. Chem. 273, 58855891.
  • Forrester MT, Foster MW, Benhar M, Stamler JS (2009) Detection of protein S-nitrosylation with the biotin-switch technique. Meth. Free Radical Biol. Med. 46, 119126.
  • Fraysse B, Desaphy JF, Rolland JF, Pierno S, Liantonio A, Giannuzzi V, Camerino C, Didonna MP, Cocchi D, De Luca A, et al. (2006) Fiber type-related changes in rat skeletal muscle calcium homeostasis during aging and restoration by growth hormone. Neurobiol. Dis. 21, 372380.
  • Ghaly A, Marsh DR (2010) Aging-associated oxidative stress modulates the acute inflammatory response in skeletal muscle after contusion injury. Exp. Gerontol. 45, 381388.
  • Goll DE, Thompson VF, Li H, Wei W, Cong J (2003) The calpain system. Physiol. Rev. 83, 731801.
  • Gutmann E, Hanzlikova V (1965) Age changes of motor endplates in muscle fibres of the rat. Gerontologia 11, 1224.
  • Holloszy JO, Chen M, Cartee GD, Young JC (1991) Skeletal muscle atrophy in old rats: differential changes in the three fiber types. Mech. Ageing Dev. 60, 199213.
  • Hotchkiss RS, Karl IE (1994) Dantrolene ameliorates the metabolic hallmarks of sepsis in rats and improves survival in a mouse model of endotoxemia. Proc. Natl. Acad. Sci. U.S.A. 91, 30393043.
  • Ingalls CP, Warren GL, Armstrong RB (1999) Intracellular Ca2+ transients in mouse soleus muscle after hindlimb unloading and reloading. J. Appl. Physiol. 87, 386390.
  • Ishiura S, Sugita H, Suzuki K, Imahori K (1979) Studies of a calcium-activated neutral protease from chicken skeletal muscle. II. Substrate specificity. J. Biochem. 86, 579581.
  • Koh TJ, Tidball JG (2000) Nitric oxide inhibits calpain-mediated proteolysis of talin in skeletal muscle cells. Am. J. Physiol. 279, C806C812.
  • Liu Z, Cao C, Gao X, Ma Q, Ren J, Xue Y (2011) GPS-CCD: GPS-CCD: A novel computational program for the prediction of calpain cleavage sites. PLoS ONE 6, e19001.
  • Maejima Y, Susumu A, Morikawa K, Ito H, Isobe M (2005) Nitric oxide inhibits myocardial apoptosis by preventing caspase-3 activity via S-nitrosylation. J. Mol. Cell. Cardiol. 38, 163174.
  • McGinnis KM, Gnegy ME, Park YH, Mukerjee N, Wang KK (1999) Procaspase-3 and poly(ADP)ribose polymerase (PARP) are calpain substrates. Biochem. Biophys. Res. Commun. 263, 9499.
  • Meng H, Leddy JJ, Holland P, Tuana BS (1996) The association of cardiac dystrophin with myofibrils/Z-disc regions in cardiac muscle suggests a novel role in the contractile apparatus. J. Biol. Chem. 271, 1236412371.
  • Nelson WB, Smuder AJ, Hudson MB, Talbert EE, Powers SK (2012) Cross-talk between the calpain and caspase-3 proteolytic systems in the diaphragm during prolonged mechanical ventilation. Crit. Care Med. 40, 18571863.
  • Nguyen HX, Tidball JG (2003) Expression of a muscle-specific, nitric oxide synthase transgene prevents muscle membrane injury and reduces muscle inflammation during modified muscle use in mice. J. Physiol. 550, 347356.
  • Reddy MK, Etlinger JD, Rabinowitz M, Fischman DA, Zak R (1975) Removal of Z-lines and alpha-actinin from isolated myofibrils by a calcium-activated neutral protease. J. Biol. Chem. 250, 42784284.
  • Renganathan M, Messi ML, Delbono O (1997) Dihydropyridine receptor-ryanodine receptor uncoupling in aged skeletal muscle. J. Membr. Biol. 157, 247253.
  • Rossig L, Fichtlscherer B, Breitschopf K, Haendeler J, Zeiher AM, Mulsch A, Dimmeler S (1999) Nitric oxide inhibits caspase-3 by S-nitrosation in vivo. J. Biol. Chem. 274, 68236826.
  • Sellman JE, DeRuisseau KC, Betters JL, Lira VA, Soltow QA, Selsby JT, Criswell DS (2006) In vivo inhibition of nitric oxide synthase impairs upregulation of contractile protein mRNA in overloaded plantaris muscle. J. Appl. Physiol. 100, 258265.
  • Shiao T, Fond A, Deng B, Wehling-Henricks M, Adams ME, Froehner SC, Tidball JG (2004) Defects in neuromuscular junction structure in dystrophic muscle are corrected by expression of a NOS transgene in dystrophin-deficient muscles, but not in muscles lacking alpha- and beta1-syntrophins. Human Mol. Genet. 13, 18731884.
  • Smuder AJ, Kavazis AN, Hudson MB, Nelson WB, Powers SK (2010) Oxidation enhances myofibrillar protein degradation via calpain and caspase-3. Free Radic. Biol. Med. 49, 11521160.
  • Solomon V, Goldberg AL (1996) Importance of the ATP-ubiquitin-proteasome pathway in the degradation of soluble and myofibrillar proteins in rabbit muscle extracts. J. Biol. Chem. 271, 2669026697.
  • Supinski GS, Wang W, Callahan LA (2009) Caspase and calpain activation both contribute to sepsis-induced diaphragmatic weakness. J. Appl. Physiol. 107, 13891396.
  • Suzuki N, Motohashi N, Uezumi A, Fukada S, Yoshimura T, Itoyama Y, Aoki M, Miyagoe-Suzuki Y, Takeda S (2007) NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. J. Clin. Invest. 117, 24682476.
  • Tidball JG, Spencer M (2002) Expression of a calpastatin transgene slows muscle wasting and obviates changes in myosin isoform expression during murine muscle disuse. J. Physiol. 545, 819828.
  • Tidball JG, Lavergne E, Lau KS, Spencer MJ, Stull JT, Wehling M (1998) Mechanical loading regulates NOS expression and activity in developing and adult skeletal muscle. Amer. J. Physiol. 275, C260C266.
  • Villalta SA, Rinaldi C, Deng B, Liu G, Fedor B, Tidball JG (2011) Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype. Human Mol. Genet. 20, 790805.
  • Volpi E, Nazemi R, Fujita S (2004) Muscle tissue changes with aging. Curr. Opin. Clin. Nutr. Metab. Care 7, 405410.
  • Wang KK, Posmantur R, Nadimpalli R, Nath R, Mohan P, Nixon RA, Talanian RV, Keegan M, Herzog L, Allen H (1998) Caspase-mediated fragmentation of calpain inhibitor protein calpastatin during apoptosis. Arch. Biochem. Biophys. 356, 187196.
  • Wehling M, Spencer M, Tidball JG (2001) A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx mice. J. Cell Biol. 155, 123131.
  • Wei W, Fareed MU, Evenson A, Menconi MJ, Yang H, Petkova V, Hasselgren P (2004) Sepsis stimulates calpain activity in skeletal muscle by decreasing calpastatin activity but does not activate caspase-3. Am. J. Physiol. 288, R580R590.
  • Williams AB, Decourten-Myers GM, Fischer JE, Luo G, Sun X, Hasselgren PO (1999) Sepsis stimulates release of myofilaments in skeletal muscle by a calcium-dependent mechanism. FASEB J. 13, 14351443.