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Early programming and environmental epigenetics of asthma.
Mon.schr. Kinderheilkd. 158, 142-148 (2010)
The term "early programming" describes the mechanisms by which specific environmental exposures during critical periods of early development have a long-term impact on a child's disease risks in later life. Moreover, this effect is passed on across generations even after discontinuation of the exposure. Understanding these mechanisms offers the potential of targeted therapeutic reprogramming in order to prevent asthma. Programming of diseases is caused by epigenetic mechanisms. These are heritable gene modifications that leave the DNA sequence untouched but can nonetheless be transferred to the next generation. The influence of prenatal exposures during pregnancy, such as nutrition, immune stimulatory substances or tobacco smoke on a child's risk for asthma has been highlighted in epidemiologic studies. Only recently, it was shown for the first time that exposure to nutrients or exhaust fumes in utero leads to epigenetic changes and is directly associated with asthma risk in children. This risk was transmitted across two generations. The potential of this new insight into epigenetically mediated early programming of asthma offers novel opportunities for the development of pre-symptomatic preventive strategies.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
0.308
0.160
1
3
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Asthma; Programming; Epigenetic; Prenatal phase; Environment
Sprache
englisch
Veröffentlichungsjahr
2010
HGF-Berichtsjahr
2010
ISSN (print) / ISBN
0026-9298
e-ISSN
1433-0474
Zeitschrift
Monatsschrift Kinderheilkunde
Quellenangaben
Band: 158,
Heft: 2,
Seiten: 142-148
Verlag
Springer
Verlagsort
New York
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Lung Health and Immunity (LHI)
POF Topic(s)
30202 - Environmental Health
Forschungsfeld(er)
Lung Research
PSP-Element(e)
G-501600-003
Erfassungsdatum
2010-12-31