Author: Ravlić S1, Vidaček NŠ2, Nanić L3, Laganović M4, Slade N5, Jelaković B6, Rubelj I7
Affiliation:
1Laboratory for molecular and cellular biology, Division of Molecular Biology, RBI, Zagreb, Croatia. Electronic address: Sanda.Ravlic@irb.hr.
2Laboratory for molecular and cellular biology, Division of Molecular Biology, RBI, Zagreb, Croatia. Electronic address: nskrobot@irb.hr.
3Laboratory for molecular and cellular biology, Division of Molecular Biology, RBI, Zagreb, Croatia. Electronic address: Lucia.Nanic@irb.hr.
4Department for Nephrology, Hypertension, Dialysis and Transplantation, University Hospital Centre Zagreb, Zagreb, Croatia. Electronic address: mlaganovic@gmail.com.
5Laboratory for protein dynamics, Division of Molecular Medicine, RBI, Zagreb, Croatia. Electronic address: Neda.Slade@irb.hr.
6Department for Nephrology, Hypertension, Dialysis and Transplantation, University Hospital Centre Zagreb, Zagreb, Croatia. Electronic address: jelakovicbojan@gmail.com.
7Laboratory for molecular and cellular biology, Division of Molecular Biology, RBI, Zagreb, Croatia. Electronic address: rubelj@irb.hr.
Conference/Journal: Mech Ageing Dev.
Date published: 2017 Aug 25
Other:
Pages: S0047-6374(17)30161-6 , Special Notes: doi: 10.1016/j.mad.2017.08.014. [Epub ahead of print] , Word Count: 121
Advances in epigenetics now enable us to better understand environmental influences on the genetic background of human diseases. This refers especially to fetal development where an adverse intrauterine environment impacts oxygen and nutrient supply to the fetus. Recently, differences in telomere length and telomere loss dynamics among individuals born with intrauterine growth restriction compared to normal controls have been described. In this paper we propose possible molecular mechanisms that (pre)program telomere epigenetics during pregnancy. This programming sets differences in telomere lengths and dynamics of telomere shortening in adulthood and therefore dictates the dynamics of aging and morbidity in later life.
Copyright © 2017 Elsevier B.V. All rights reserved.
KEYWORDS: Epigenetics; aging; cardiovascular disease; fetal development; longevity; telomere
PMID: 28847485 DOI: 10.1016/j.mad.2017.08.014