PMID- 23873298
OWN - NLM
STAT- MEDLINE
DCOM- 20140211
LR  - 20220409
IS  - 1422-0067 (Print)
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 14
IP  - 7
DP  - 2013 Jul 18
TI  - Defective homocysteine metabolism: potential implications for skeletal muscle 
      malfunction.
PG  - 15074-91
LID - 10.3390/ijms140715074 [doi]
AB  - 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.
FAU - Veeranki, Sudhakar
AU  - Veeranki S
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY 40202, USA. s0veer02@louisville.edu
FAU - Tyagi, Suresh C
AU  - Tyagi SC
LA  - eng
GR  - R01 HL074185/HL/NHLBI NIH HHS/United States
GR  - R01 HL108621/HL/NHLBI NIH HHS/United States
GR  - HL-74185/HL/NHLBI NIH HHS/United States
GR  - HL-108621/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20130718
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Endoplasmic Reticulum Stress
MH  - Homocysteine/*metabolism
MH  - Humans
MH  - Hyperhomocysteinemia/metabolism/*physiopathology
MH  - Methylation
MH  - Muscle, Skeletal/*metabolism
MH  - Nitric Oxide/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, G-Protein-Coupled/metabolism
MH  - Signal Transduction
PMC - PMC3742288
EDAT- 2013/07/23 06:00
MHDA- 2014/02/12 06:00
PMCR- 2013/07/01
CRDT- 2013/07/23 06:00
PHST- 2013/05/27 00:00 [received]
PHST- 2013/06/24 00:00 [revised]
PHST- 2013/07/11 00:00 [accepted]
PHST- 2013/07/23 06:00 [entrez]
PHST- 2013/07/23 06:00 [pubmed]
PHST- 2014/02/12 06:00 [medline]
PHST- 2013/07/01 00:00 [pmc-release]
AID - ijms140715074 [pii]
AID - ijms-14-15074 [pii]
AID - 10.3390/ijms140715074 [doi]
PST - epublish
SO  - Int J Mol Sci. 2013 Jul 18;14(7):15074-91. doi: 10.3390/ijms140715074.