ArticleRenal failure2017
Pin1 and secondary hyperparathyroidism of chronic kidney disease: gene polymorphisms and protein levels.
Article in Renal failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease.Journal of endocrinological investigation · 2026Review
- The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024Review
- A Molecular Insight of the Role of PIN-1 Promoter Polymorphism (- 667C > T; rs2233679) in Chronic Kidney Disease Patients with Secondary Hyperparathyroidism.Indian journal of clinical biochemistry : IJCB · 2022Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPeptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (Pin1) is a key regulator of PTH mRNA stability. Secondary hyperparathyroidism (SHPT), which is characterized by elevated serum PTH levels, is a common complication of CKD. We investigated the possible associations between CKD with SHPT (CKD SHPT) and single-nucleotide polymorphisms of the Pin1 gene and compared the levels of the Pin1 protein in the CKD SHPT patients with those of the controls.
methodsThe study group included 251 CKD SHPT patients and 61 controls. One putative functional SNP (single nucleotide polymorphism) in the Pin1 promoter (rs2233679C > T: c.-667C > T) is the main object. Genotyping was performed on purified DNA using polymerase chain reaction-restriction (PCR) and restriction fragment length polymorphisms (RFLP). The levels of Pin1 were measured in serum using an enzyme-linked immunosorbent assay.
resultsGenotyping showed that CT + TT in the Pin1 promoter was significantly more common in the CKD SHPT group than in the control group (p<.05). The correlation analysis demonstrated that a significant difference in the C to T transition in the Pin1 promoter contributed to CKD SHPT (χ
conclusionThe -667T genetic variants in the Pin1 promoter contribute to an increased risk of CKD SHPT and may be biomarkers of susceptibility to CKD SHPT.
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