Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia

Anuradha Kalani, Pradip K. Kamat, Michael J. Voor, Suresh C. Tyagi, Neetu Tyagi

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)89-98
Number of pages10
JournalMolecular and Cellular Biochemistry
Volume395
Issue number1-2
DOIs
StatePublished - Oct 2014
Externally publishedYes

Keywords

  • Bone
  • DNA methylation
  • Epigenetics
  • Homocysteine
  • Mitochondria

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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