Genetic variation in CARD8, a gene coding for an NLRP3 inflammasome-associated protein, alters the genetic risk for diabetic nephropathy in the context of type 2 diabetes mellitus.
Fotis TsetsosAthanasios RoumeliotisXanthippi A TsekmekidouSophia AlexoudaRoumeliotis StefanosMarios TheodoridisElias ThodisStylianos PanagoutsosNikolaos PapanasDimitrios PapazoglouKalliopi KotsaJohn G YovosEfstratios MaltezosPloumis PassadakisPeristera PaschouMarianthi GeorgitsiPublished in: Diabetes & vascular disease research (2021)
CARD8 acts as an NLRP3, NF-κB and caspase-1 inhibitor; perhaps, alterations in the cross-talk between CARD8, NF-κB, and NLRP3, which could affect the pro-inflammatory environment in T2DM, render diabetic carriers of certain common CARD8 variants potentially less likely to develop T2DM-related pro-inflammatory responses followed by DN. These preliminary, yet novel, observations will require validation in larger cohorts from several ethnic groups.
Keyphrases
- nlrp inflammasome
- diabetic nephropathy
- copy number
- signaling pathway
- lps induced
- genome wide
- oxidative stress
- type diabetes
- pi k akt
- nuclear factor
- cell death
- induced apoptosis
- gene expression
- glycemic control
- anti inflammatory
- adipose tissue
- wound healing
- immune response
- transcription factor
- endoplasmic reticulum stress
- genome wide identification