Int. J. Mol. Sci. 2013, 14(7), 15074-15091; doi:10.3390/ijms140715074

Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction

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Received: 27 May 2013; in revised form: 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)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: 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.
Keywords: hyperhomocysteinemia; homocysteine; inflammation; muscle; dystrophy; degeneration; ROS; GPCR; NO; ER stress
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MDPI and ACS Style

Veeranki, S.; Tyagi, S.C. Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction. Int. J. Mol. Sci. 2013, 14, 15074-15091.

AMA Style

Veeranki S, Tyagi SC. Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction. International Journal of Molecular Sciences. 2013; 14(7):15074-15091.

Chicago/Turabian Style

Veeranki, Sudhakar; Tyagi, Suresh C. 2013. "Defective Homocysteine Metabolism: Potential Implications for Skeletal Muscle Malfunction." Int. J. Mol. Sci. 14, no. 7: 15074-15091.

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