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Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction

Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA
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Int. J. Mol. Sci. 2013, 14(7), 15074-15091; https://doi.org/10.3390/ijms140715074
Received: 27 May 2013 / Revised: 24 June 2013 / Accepted: 11 July 2013 / Published: 18 July 2013
(This article belongs to the Special Issue Redox Signaling in Biology and Patho-Biology)
Hyperhomocysteinemia (HHcy) is a systemic medical condition and has been attributed to multi-organ pathologies. Genetic, nutritional, hormonal, age and gender differences are involved in abnormal homocysteine (Hcy) metabolism that produces HHcy. Homocysteine is an intermediate for many key processes such as cellular methylation and cellular antioxidant potential and imbalances in Hcy production and/or catabolism impacts gene expression and cell signaling including GPCR signaling. Furthermore, HHcy might damage the vagus nerve and superior cervical ganglion and affects various GPCR functions; therefore it can impair both the parasympathetic and sympathetic regulation in the blood vessels of skeletal muscle and affect long-term muscle function. Understanding cellular targets of Hcy during HHcy in different contexts and its role either as a primary risk factor or as an aggravator of certain disease conditions would provide better interventions. In this review we have provided recent Hcy mediated mechanistic insights into different diseases and presented potential implications in the context of reduced muscle function and integrity. Overall, the impact of HHcy in various skeletal muscle malfunctions is underappreciated; future studies in this area will provide deeper insights and improve our understanding of the association between HHcy and diminished physical function. View Full-Text
Keywords: hyperhomocysteinemia; homocysteine; inflammation; muscle; dystrophy; degeneration; ROS; GPCR; NO; ER stress hyperhomocysteinemia; homocysteine; inflammation; muscle; dystrophy; degeneration; ROS; GPCR; NO; ER stress
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Veeranki, S.; Tyagi, S.C. Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction. Int. J. Mol. Sci. 2013, 14, 15074-15091.

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