Roles of the Chr.9p21.3 Locus in Regulating Inflammation and Implications for Anti-Inflammatory Drug Target Identification
Standard
Roles of the Chr.9p21.3 Locus in Regulating Inflammation and Implications for Anti-Inflammatory Drug Target Identification. / Aarabi, Ghazal; Zeller, Tanja; Heydecke, Guido; Munz, Matthias; Schäfer, Arne; Seedorf, Udo.
In: FRONT CARDIOVASC MED, Vol. 5, No. 47, 01.05.2018.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Roles of the Chr.9p21.3 Locus in Regulating Inflammation and Implications for Anti-Inflammatory Drug Target Identification
AU - Aarabi, Ghazal
AU - Zeller, Tanja
AU - Heydecke, Guido
AU - Munz, Matthias
AU - Schäfer, Arne
AU - Seedorf, Udo
PY - 2018/5/1
Y1 - 2018/5/1
N2 - Periodontitis (PD) is a common gingival infectious disease caused by an over-aggressive inflammatory reaction to dysbiosis of the oral microbiome. The disease induces a profound systemic inflammatory host response, that triggers endothelial dysfunction and pro-thrombosis and thus may aggravate atherosclerotic vascular disease and its clinical complications. Recently, a risk haplotype at the ANRIL/CDKN2B-AS1 locus on chromosome 9p21.3, that is not only associated with coronary artery disease / myocardial infarction (CAD/MI) but also with PD, could be identified by genome-wide association studies. The locus encodes ANRIL - a long non-coding RNA (lncRNA) which, like other lncRNAs, regulates genome methylation via interacting with specific DNA sequences and proteins, such as DNA methyltranferases and polycomb proteins, thereby affecting expression of multiple genes by cis and trans mechanisms. Here, we describe ANRIL regulated genes and metabolic pathways and discuss implications of the findings for target identification of drugs with potentially anti-inflammatory activity in general.
AB - Periodontitis (PD) is a common gingival infectious disease caused by an over-aggressive inflammatory reaction to dysbiosis of the oral microbiome. The disease induces a profound systemic inflammatory host response, that triggers endothelial dysfunction and pro-thrombosis and thus may aggravate atherosclerotic vascular disease and its clinical complications. Recently, a risk haplotype at the ANRIL/CDKN2B-AS1 locus on chromosome 9p21.3, that is not only associated with coronary artery disease / myocardial infarction (CAD/MI) but also with PD, could be identified by genome-wide association studies. The locus encodes ANRIL - a long non-coding RNA (lncRNA) which, like other lncRNAs, regulates genome methylation via interacting with specific DNA sequences and proteins, such as DNA methyltranferases and polycomb proteins, thereby affecting expression of multiple genes by cis and trans mechanisms. Here, we describe ANRIL regulated genes and metabolic pathways and discuss implications of the findings for target identification of drugs with potentially anti-inflammatory activity in general.
KW - Journal Article
U2 - 10.3389/fcvm.2018.00047
DO - 10.3389/fcvm.2018.00047
M3 - SCORING: Journal article
C2 - 29868613
VL - 5
JO - FRONT CARDIOVASC MED
JF - FRONT CARDIOVASC MED
SN - 2297-055X
IS - 47
ER -