CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene-Gene Interactions Are Associated with Restenosis after Coronary Stenting

Biomolecules. 2022 May 31;12(6):765. doi: 10.3390/biom12060765.

Abstract

In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene−gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs2071592 T/A, LTA rs1800683 G/A, CASP1 rs501192 A/G, and CASP1 rs580253 A/G) were performed by 5’exonuclease TaqMan assays in 219 patients: 66 patients with restenosis and 153 without restenosis. The distribution of rs2239527 C/G, rs2071592 T/A, and rs1800683 G/A polymorphisms was similar in patients with and without restenosis. Nonetheless, under recessive (OR = 2.73, pCRes = 0.031) and additive models (OR = 1.65, pCAdd = 0.039), the AA genotype of the rs501192 A/G polymorphism increased the restenosis risk. Under co-dominant, dominant, recessive, and additive models, the AA genotype of the rs580253 A/G was associated with a high restenosis risk (OR = 5.38, pCCo-Dom = 0.003; OR = 2.12, pCDom = 0.031; OR = 4.32, pCRes = 0.001; and OR = 2.16, 95%CI: 1.33−3.52, pCAdd = 0.001, respectively). In addition, we identified an interaction associated with restenosis susceptibility: BAT1-NFKBIL1-LTA-CASP1 (OR = 9.92, p < 0.001). In summary, our findings demonstrate that the rs501192 A/G and rs580253 A/G polymorphisms, as well as the gene−gene interactions between BAT1-NFKBIL1-LTA-CASP1, are associated with an increased restenosis risk after coronary stenting.

Keywords: genetics; polymorphisms; restenosis; susceptibility.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Caspase 1* / genetics
  • Coronary Restenosis* / genetics
  • Epistasis, Genetic
  • Genetic Predisposition to Disease*
  • Humans
  • Polymorphism, Single Nucleotide

Substances

  • Caspase 1

Grants and funding

This research was funded by the Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, México (Number project-22-1288).