Abstract
Objective: Cystatin C, a marker of atherosclerosis, is encoded by CST3. We aimed to evaluate whether two single-nucleotide polymorphisms (SNPs) of CST3 are correlated with large-artery atherosclerotic stroke (LAAS) and prognosis.Methods: This subgroup analysis of the Third China National Stroke Registry (CNSR-III) enrolled acute ischemic stroke (AIS) patients within 7 days from August 2015 to March 2018 in China. rs13038305 and rs911119 of CST3 were selected based on the strong association with cystatin C concentration.Results: Two loci of CST3 (rs13038305 and rs911119) were analyzed in 3,833 ischemic stroke patients. Carriers of T allele in rs13038305 and C allele in rs911119 tend to have lower serum cystatin C levels (p < 0.05). Compared with C/C as a reference in rs13038305, odds ratio (OR) of T/T was 0.486, 95% CI 0.237–0.994, p = 0.048. Per C allele of rs13038305 also showed an increased level of low-density lipoprotein cholesterol (LDL-C), β (95% CI) was 1.335 (1.008–1.250), p = 0.044. No correlation was found between the selected SNPs and stroke prognosis (functional outcome, recurrence, and mortality).Conclusions: Carriers of the T allele in rs13038305 tend to have a lower proportion of LAAS. rs13038305 and rs911119 polymorphisms were likely to affect cystatin C concentration independently of kidney function.
Highlights
Cystatin C (CysC, encoded by CST3 on 20p11.21) is a candidate marker of glomerular filtration rate [1, 2]
We found that carriers of the T allele of single-nucleotide polymorphisms (SNPs) rs13038305 tend to have a lower proportion of Largeartery atherosclerotic stroke (LAAS)
The possible reason is that large-artery stenosis is not the only factor leading to LAAS, and our classification method to assess intracranial and extracranial large-vessel stenosis may miss some detailed information about the degree of vascular stenosis and the state of atherosclerotic plaque
Summary
Cystatin C (CysC, encoded by CST3 on 20p11.21) is a candidate marker of glomerular filtration rate [1, 2]. As a competitive inhibitor of cysteine proteases, CysC is involved in the process of atherosclerotic plaque remodeling [3] and independently associated with cerebral artery stenosis and prognosis in stroke patients [4]. The imbalance expression between CysC and cysteine proteases is a key factor of atherosclerosis. The effects of CysC on metabolic syndrome and atherosclerosis-related factors have been confirmed in observational studies [5], the underlying mechanism is still unclear [2, 6]. The causal involvement or directionality of any causal effect on artery stenosis and ischemic stroke is yet to be proven [7].
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