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Statements

Subject Item
n2:RIV%2F00209805%3A_____%2F14%3A%230000519%21RIV15-MSM-00209805
rdf:type
n3:Vysledek skos:Concept
rdfs:seeAlso
http://dx.doi.org/10.1016/j.molcel.2014.02.035
dcterms:description
In addition to its anticancer function, p53 (regulated by MDM2) has recently been shown to control intracellular metabolic processes. It participates in the regulation of glucose, fatty and amino acid and purine metabolism, influences mitochondrial integrity and oxidative phosphorylation, insulin sensitivity, antioxidant response and autophagy. With respect to the possible impact of genetic variability in p53 and MDM2 on metabolic compensation the aim of the study was to analyse the effect of common germ line Single Nucleotide Polymorphisms (SNPs) - Arg72Pro in the TP53 and SNP309 in the MDM2 - on the progression of Diabetic Nephropathy (DN), cardiovascular morbidity and mortality and all-cause mortality in Type 2 Diabetes Mellitus (T2DM) subjects. The cross-sectional study comprised a total of 309 (a sum of 155 and 154) unrelated Caucasian diabetic patients with diabetes duration at least 10 years and variable renal function at baseline (309, mean age was 67.2 ± 10.8 years). The stage of diabetic nephropathy was defined according to the urinary albumin excretion and glomerular filtration rate. We found significant difference between CG+GG vs. CC genotypes of the p53 Arg72Pro SNP for DN progression (P=0.046, log-rank test). Carriers of genotypes containing G allele (previously associated with susceptibility to T2DM) had faster progression of DN than CC genotype carriers. We did not find any significant difference between genotypes of MDM2 SNP for any of the end-points studied. Presented findings in general support the role of p53 in the pathogenesis of metabolic diseases, namely progression of hyperglycemia-related morbidity. Nevertheless, further studies are warranted to elucidate the eventual causal involvement of p53 pathway in the development of diabetic complications. In addition to its anticancer function, p53 (regulated by MDM2) has recently been shown to control intracellular metabolic processes. It participates in the regulation of glucose, fatty and amino acid and purine metabolism, influences mitochondrial integrity and oxidative phosphorylation, insulin sensitivity, antioxidant response and autophagy. With respect to the possible impact of genetic variability in p53 and MDM2 on metabolic compensation the aim of the study was to analyse the effect of common germ line Single Nucleotide Polymorphisms (SNPs) - Arg72Pro in the TP53 and SNP309 in the MDM2 - on the progression of Diabetic Nephropathy (DN), cardiovascular morbidity and mortality and all-cause mortality in Type 2 Diabetes Mellitus (T2DM) subjects. The cross-sectional study comprised a total of 309 (a sum of 155 and 154) unrelated Caucasian diabetic patients with diabetes duration at least 10 years and variable renal function at baseline (309, mean age was 67.2 ± 10.8 years). The stage of diabetic nephropathy was defined according to the urinary albumin excretion and glomerular filtration rate. We found significant difference between CG+GG vs. CC genotypes of the p53 Arg72Pro SNP for DN progression (P=0.046, log-rank test). Carriers of genotypes containing G allele (previously associated with susceptibility to T2DM) had faster progression of DN than CC genotype carriers. We did not find any significant difference between genotypes of MDM2 SNP for any of the end-points studied. Presented findings in general support the role of p53 in the pathogenesis of metabolic diseases, namely progression of hyperglycemia-related morbidity. Nevertheless, further studies are warranted to elucidate the eventual causal involvement of p53 pathway in the development of diabetic complications.
dcterms:title
HDMX folds the nascent p53 mRNA following activation by the ATM kinase HDMX folds the nascent p53 mRNA following activation by the ATM kinase
skos:prefLabel
HDMX folds the nascent p53 mRNA following activation by the ATM kinase HDMX folds the nascent p53 mRNA following activation by the ATM kinase
skos:notation
RIV/00209805:_____/14:#0000519!RIV15-MSM-00209805
n4:aktivita
n13:P
n4:aktivity
P(ED2.1.00/03.0101)
n4:cisloPeriodika
3
n4:dodaniDat
n8:2015
n4:domaciTvurceVysledku
n19:3803066
n4:druhVysledku
n11:J
n4:duvernostUdaju
n18:S
n4:entitaPredkladatele
n17:predkladatel
n4:idSjednocenehoVysledku
18824
n4:idVysledku
RIV/00209805:_____/14:#0000519
n4:jazykVysledku
n7:eng
n4:klicovaSlova
HDMX; ATM kinase; p53 mRNA
n4:klicoveSlovo
n14:HDMX n14:p53%20mRNA n14:ATM%20kinase
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[BAD9D7DD9D48]
n4:nazevZdroje
Molecular cell
n4:obor
n6:EB
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
6
n4:projekt
n12:ED2.1.00%2F03.0101
n4:rokUplatneniVysledku
n8:2014
n4:svazekPeriodika
54
n4:tvurceVysledku
Ponnuswamy, Anand
n4:wos
000336026900016
s:issn
1097-2765
s:numberOfPages
12
n10:doi
10.1016/j.molcel.2014.02.035