Oxidative Stress Genes in Diabetes Mellitus Type 2: Association with Diabetic Kidney Disease.
Adult
Autoantigens
/ genetics
Case-Control Studies
Diabetes Mellitus, Type 2
/ complications
Diabetic Nephropathies
/ etiology
Female
Genome-Wide Association Study
Humans
Iodide Peroxidase
/ genetics
Iron-Binding Proteins
/ genetics
Male
Middle Aged
Osteopontin
/ genetics
Oxidative Stress
/ genetics
Polymorphism, Single Nucleotide
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2021
2021
Historique:
received:
24
05
2021
accepted:
21
08
2021
entrez:
21
9
2021
pubmed:
22
9
2021
medline:
27
1
2022
Statut:
epublish
Résumé
Diabetic type 2 patients compared to nondiabetic patients exhibit an increased risk of developing diabetic kidney disease (DKD), the leading cause of end-stage renal disease. Hyperglycemia, hypertension, oxidative stress (OS), and genetic background are some of the mechanisms and pathways implicated in DKD pathogenesis. However, data on OS pathway susceptibility genes show limited success and conflicting or inconclusive results. Our study is aimed at exploring OS pathway genes and variants which could be associated with DKD. We recruited 121 diabetes mellitus type 2 (DM2) patients with DKD (cases) and 220 DM2, non-DKD patients (control) of Greek origin and performed a case-control association study using genome-wide association data. PLINK and EIGENSOFT were used to analyze the data. Our results indicate 43 single nucleotide polymorphisms with their 21 corresponding genes on the OS pathway possibly contributing or protecting from DKD: SPP1, TPO, TTN, SGO2, NOS3, PDLIM1, CLU, CCS, GPX4, TXNRD2, EPHX2, MTL5, EPX, GPX3, ALOX12, IPCEF1, GSTA, OXR1, GPX6, AOX1, and PRNP. Therefore, a genetic OS background might underlie the complex pathogenesis of DKD in DM2 patients.
Identifiants
pubmed: 34545296
doi: 10.1155/2021/2531062
pmc: PMC8448992
doi:
Substances chimiques
Autoantigens
0
Iron-Binding Proteins
0
SPP1 protein, human
0
Osteopontin
106441-73-0
TPO protein, human
EC 1.11.1.7
Iodide Peroxidase
EC 1.11.1.8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2531062Informations de copyright
Copyright © 2021 Athanasios Roumeliotis et al.
Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
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