PMID- 24939359
OWN - NLM
STAT- MEDLINE
DCOM- 20151029
LR  - 20211021
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Print)
IS  - 0300-8177 (Linking)
VI  - 395
IP  - 1-2
DP  - 2014 Oct
TI  - Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia.
PG  - 89-98
LID - 10.1007/s11010-014-2114-3 [doi]
AB  - Increased levels of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy), is 
      an independent risk factor of various diseases. Clinical studies report that 
      people born with severe HHcy develop skeletal malformations with weaker bone. 
      Studies also report that altered mitochondrial dynamics and altered epigenetics 
      contribute to weaker bones and bone diseases. Although Hcy-induced mitochondrial 
      dysfunction has been shown to affect bone metabolism, the role of mitochondrial 
      epigenetics (mito-epigenetics) has not been studied in bones. The epigenetics in 
      mitochondria is interesting as the mitochondrial genome size is small (16 kb) 
      with fewer CpG, and without histones and introns. Recently, fascinating works on 
      epigenetics along with the discovery of histone-like proteins in mitochondria are 
      giving exciting areas for novel studies on mitochondria epigenetics. There are 
      mutual cause and effect relationships between bone, mitochondria, Hcy, and 
      epigenetics, but unfortunately, studies are lacking that describe the involvement 
      of all these together in bone disease progression. This review describes the 
      reciprocal relationships and mechanisms of Hcy-bone-mitochondria-epigenetics 
      along with a short discussion of techniques which could be employed to assess 
      Hcy-induced anomaly in bone, mediated through alterations in mito-epigenetics.
FAU - Kalani, Anuradha
AU  - Kalani A
AD  - Department of Physiology and Biophysics, School of Medicine, Health Sciences 
      Centre, A-1201, University of Louisville, 500 South Preston Street, Louisville, 
      KY, 40202, USA.
FAU - Kamat, Pradip K
AU  - Kamat PK
FAU - Voor, Michael J
AU  - Voor MJ
FAU - Tyagi, Suresh C
AU  - Tyagi SC
FAU - Tyagi, Neetu
AU  - Tyagi N
LA  - eng
GR  - R01 NS084823/NS/NINDS NIH HHS/United States
GR  - NS-084823-SCT/SC/NCI NIH HHS/United States
GR  - HL71010-NT/HL/NHLBI NIH HHS/United States
GR  - R01 HL107640/HL/NHLBI NIH HHS/United States
GR  - R01 HL071010/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20140618
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
SB  - IM
MH  - Animals
MH  - *Bone Remodeling
MH  - Epigenesis, Genetic
MH  - Genome, Mitochondrial
MH  - Humans
MH  - Hyperhomocysteinemia/genetics/*pathology
MH  - Mitochondria/*genetics/pathology
PMC - PMC4134425
MID - NIHMS606306
COIS- Conflict of Interest: The authors declared no conflict of interest.
EDAT- 2014/06/19 06:00
MHDA- 2015/10/30 06:00
PMCR- 2015/10/01
CRDT- 2014/06/19 06:00
PHST- 2014/03/18 00:00 [received]
PHST- 2014/06/02 00:00 [accepted]
PHST- 2014/06/19 06:00 [entrez]
PHST- 2014/06/19 06:00 [pubmed]
PHST- 2015/10/30 06:00 [medline]
PHST- 2015/10/01 00:00 [pmc-release]
AID - 10.1007/s11010-014-2114-3 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2014 Oct;395(1-2):89-98. doi: 10.1007/s11010-014-2114-3. Epub 
      2014 Jun 18.