Abstract
Pathological cardiac hypertrophy is an independent risk factor for chronic heart failure. Casein kinase-2 interacting protein-1 (CKIP-1) can inhibit pathological cardiac hypertrophy. Therefore, we investigated whether CKIP-1 nonsynonymous polymorphism rs2306235 (Pro21Ala) contributes to risk and prognosis of chronic heart failure in a Chinese population.A total of 923 adult patients with chronic heart failure and 1020 age- and gender-matched healthy controls were recruited. CKIP-1 rs2306235 polymorphism was genotyped using PCR-restriction fragment length polymorphism. Additional follow-up data for 140 chronic heart failure patients was evaluated. The rs2306235 G allele was associated with an increased risk of chronic heart failure (OR = 1.38, 95% CI = 1.09-1.75, p = 0.007), especially in patients with hypertension (OR = 1.45, 95% CI = 1.09-1.75, p = 0.006) and coronary heart disease (OR = 1.41, 95% CI = 1.09-1.83, p = 0.010) after adjustment for multiple cardiovascular risk factors. However, rs2306235 polymorphism was not associated with cardiovascular mortality in chronic heart failure (p = 0.875). CKIP-1 rs2306235 polymorphism may be a risk factor for chronic heart failure in a Chinese Han population.
Highlights
Chronic heart failure (CHF) is a complex clinical syndrome with a multifactorial etiology including genetic factors [1,2,3,4,5,6]
We investigated whether Casein kinase-2 interacting protein-1 (CKIP-1) nonsynonymous polymorphism rs2306235 (Pro21Ala) contributes to risk and prognosis of chronic heart failure in a Chinese population.A total of 923 adult patients with chronic heart failure and 1020 age- and gender-matched healthy controls were recruited
This polymorphism showed no association with severity and cardiovascular mortality in CHF patients
Summary
Chronic heart failure (CHF) is a complex clinical syndrome with a multifactorial etiology including genetic factors [1,2,3,4,5,6]. The pleckstrin homology domain-containing protein casein kinase-2 interacting protein-1 (CKIP-1) was originally identified as a casein kinase-2 α-subunit (CK2α) interacting protein [7]. CKIP-1 protein contains a pleckstrin homology (PH) domain and a leucine zipper (LZ) motif, which could mediate multiple interactions between CKIP-1 and numerous cellular proteins [8]. CKIP-1 can inhibit pathological cardiac hypertrophy by promoting dephosphorylation of histone deacetylase 4 (HDAC4) through recruiting serine/threonine protein phosphatase 2A (PP2A) [22]. Cardiacspecific deficiency and overexpression of CKIP-1 exhibit hypersensitivity and resistance to pathological cardiac hypertrophy induced by pressure overload, respectively [22]. CKIP-1 protein level was sharply reduced in the hypertrophied failing human hearts [22]
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