Relationship between PPARγ Gene Polymorphisms and the Clinical Outcome of Ischemic Stroke.
First author:Xin Qiu, Ran Yan
Corresponding author:Yongjun Wang ,Zixiao Li
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Journal:ournal of Cerebral Blood Flow & Metabolism
Publication type: Original Contributions
IF(IF): 4.5
PMID: 39161254 Link To Pubmed Full text Download
Pioglitazone is one of the thiazolidinedione class of Peroxisome proliferator-activated receptor-γ (PPARγ) agonists. PPARγ belongs to the nuclear receptor superfamily, which modulatied the transcriptional regulation of many genes involved in metabolism and energyhomeostasis. PPARγ gene has been confirmed to be associated with insulin sensitivity and the risk of diabetes in different ethnic groups. Regieli et al found that the minor allele of rs1801282 in PPARγ gene has protective effect on clinical outcome in patients with manifest coronary or other vascular disease. Animal research of neuron-specific PPARγ knock-out mice also indicated PPARγ gene plays a protective role in brain injury after stroke. Limited by the small sample size, current studies have not reached definite conclusions on the relationship between PPARγ and stroke. The role of PPARγ on the prognosis of stroke is still unknown. Our study thus aimed to evaluate the association between PPARγ gene polymorphisms and the clinical outcome of acute ischemic stroke.
Continuous variables were presented as medians with interquartile ranges and categorical variables as percentages. Baseline characteristics for patients with and without PPARγrs1801282 CC/CG+GG genotype stratified by diabetes were described separately. The linkage disequilibrium block and haplotype structure were measured by D’ among the rs1801282 SNPs. Hardy-Weinberg equilibrium was evaluated with a χ2 test. All tests were 2-sided, and P < 0.05 was considered to be statistically significant. The linkage disequilibrium block and haplotype structure were estimated using the genetics package version 3.5.1 in R (R Development Core Team). All other analyses were conducted with SAS, version 9.4 (SAS Institute Inc).