TY - JOUR
T1 - Synergy of homocysteine, MicroRNA, and epigenetics
T2 - A novel therapeutic approach for stroke
AU - Kalani, Anuradha
AU - Kamat, Pradeep K.
AU - Tyagi, Suresh C.
AU - Tyagi, Neetu
N1 - Funding Information:
Acknowledgments This work was supported by NIH grant HL-107640 to NT and NS-51568 to SCT.
PY - 2013/8
Y1 - 2013/8
N2 - Homocysteine (Hcy) is a thiol-containing amino acid formed during methionine metabolism. Elevated level of Hcy is known as hyperhomocysteinemia (HHcy). HHcy is an independent risk factor for cerebrovascular diseases such as stroke, dementia, Alzheimer's disease, etc. Stroke, which is caused by interruption of blood supply to the brain, is one of the leading causes of death and disability in a number of people worldwide. The HHcy causes an increased carotid artery plaque that may lead to ischemic stroke but the mechanism is currently not well understood. Though mutations or polymorphisms in the key genes of Hcy metabolism pathway have been well elucidated in stroke, emerging evidences suggested epigenetic mechanisms equally play an important role in stroke development such as DNA methylation, chromatin remodeling, RNA editing, noncoding RNAs (ncRNAs), and microRNAs (miRNAs). However, there is no review available yet that describes the role of genetics and epigenetics during HHcy in stroke. The current review highlights the role of genetics and epigenetics in stroke during HHcy and the role of epigenetics in its therapeutics. The review also highlights possible epigenetic mechanisms, potential therapeutic molecules, putative challenges, and approaches to deal with stroke during HHcy.
AB - Homocysteine (Hcy) is a thiol-containing amino acid formed during methionine metabolism. Elevated level of Hcy is known as hyperhomocysteinemia (HHcy). HHcy is an independent risk factor for cerebrovascular diseases such as stroke, dementia, Alzheimer's disease, etc. Stroke, which is caused by interruption of blood supply to the brain, is one of the leading causes of death and disability in a number of people worldwide. The HHcy causes an increased carotid artery plaque that may lead to ischemic stroke but the mechanism is currently not well understood. Though mutations or polymorphisms in the key genes of Hcy metabolism pathway have been well elucidated in stroke, emerging evidences suggested epigenetic mechanisms equally play an important role in stroke development such as DNA methylation, chromatin remodeling, RNA editing, noncoding RNAs (ncRNAs), and microRNAs (miRNAs). However, there is no review available yet that describes the role of genetics and epigenetics during HHcy in stroke. The current review highlights the role of genetics and epigenetics in stroke during HHcy and the role of epigenetics in its therapeutics. The review also highlights possible epigenetic mechanisms, potential therapeutic molecules, putative challenges, and approaches to deal with stroke during HHcy.
KW - Brain
KW - CBS
KW - Cerebrovascular diseases
KW - Chromatin remodeling
KW - DNA methylation
KW - Epigenomics
KW - MTHFR
KW - Noncoding RNA
KW - Vascular diseases
UR - http://www.scopus.com/inward/record.url?scp=84880922774&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84880922774&partnerID=8YFLogxK
U2 - 10.1007/s12035-013-8421-y
DO - 10.1007/s12035-013-8421-y
M3 - Review article
C2 - 23430482
AN - SCOPUS:84880922774
SN - 0893-7648
VL - 48
SP - 157
EP - 168
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 1
ER -