Background And Objectives: Sclerostin, dickkopf-related protein 1 (DKK1), fibroblast growth factor-23 (FGF23) and α-klotho have been shown to play an important role in bone and vascular disease of chronic kidney disease. We aimed to evaluate the evolution of these bone markers in newly kidney transplanted patients, and whether they are associated with bone metabolism and vascular stiffness.
Design, Setting, Participants And Measurements: This is a longitudinal single-center observational cohort study. Circulating levels of Wnt/β-catenin pathway inhibitors (sclerostin, DKK1, FGF23 and α-klotho), arterial stiffness (carotid-femoral pulse-wave velocity (PWV), carotid-radial PWV, PWV ratio, augmented index) and bone parameters were assessed before (M0), and at 3 (M3) and 6 months (M6) after transplantation. Generalized estimating equations were conducted for comparative analyses between the three time points. We used a marginal structural model for repeated measures for the impact of changes in bone markers on the evolution of arterial stiffness. Multivariate linear regression analyses were performed for the associations between Wnt/β-catenin pathway inhibitors and mineral metabolism parameters.
Results: We included 79 patients (70% male; median age of 53 (44-60) years old). The levels of sclerostin (2.06 ± 1.18 ng/mL at M0 to 0.88 ± 0.29 ng/mL at M6, p ≤ 0.001), DKK1 (364.0 ± 266.7 pg/mL at M0 to 246.7 ± 149.1 pg/mL at M6, p ≤ 0.001), FGF23 (5595 ± 9603 RU/mL at M0 to 137 ± 215 RU/mL at M6, p ≤ 0.001) and α-klotho (457.6 ± 148.6 pg/mL at M0 to 109.8 ± 120.7 pg/mL at M6, p < 0.05) decreased significantly after kidney transplant. Sclerostin and FGF23 were positively associated with carotid-femoral (standardized β = 0.432, p = 0.037 and standardized β = 0.592, p = 0.005) and carotid-radial PWV (standardized β = 0.259, p = 0.029 and standardized β = 0.242, p = 0.006) throughout the 6 months of follow-up. The nature of the associations between bone markers and bone metabolism parameters varies after kidney transplant.
Conclusions: The circulating levels of Wnt/β-catenin pathway inhibitors and α-klotho significantly decrease after kidney transplantation, while sclerostin and FGF23 levels might be associated with improvement of vascular stiffness and blood pressure.
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http://dx.doi.org/10.1007/s40620-022-01563-y | DOI Listing |
Invest Ophthalmol Vis Sci
January 2025
Dr. Rolf M. Schwiete Center for Limbal Stem Cell and Congenital Aniridia Research, Homburg/Saar, Germany, Saarland University, Homburg/Saar, Germany.
Purpose: This study evaluates the microRNA (miRNA) expression profile in primary limbal epithelial cells (pLECs) of patients with aniridia.
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Discov Oncol
January 2025
Department of Ear, Nose and Throat (ENT), The First People's Hospital of Jiande, No. 599 Yanzhou Avenue, Xin'anjiang Street, Jiande, 311600, Zhejiang, China.
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Mol Cancer Res
December 2024
Kaifeng 155 Hospital, Kaifeng, Henan, China.
Cancer remains one of the most formidable challenges in the medical field in this century, largely due to its poorly understood pathogenesis. Fortunately, recent advancements in the understanding of cancer pathogenesis have helped identify more therapeutic targets for improved treatment outcomes. The WNT signaling pathways are highly conserved cascades that participate in diverse physiological processes, such as embryonic development, tissue homeostasis, and tissue regeneration.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of São Paulo Universidade de São Paulo, São Paulo, Brazil.
Background: The Down Syndrome (DS), also referred to as trisomy of chromosome 21, is a prevalent cause of intellectual disability and also contributes to the acceleration of aging, among other developmental and health concerns. Certain pathological characteristics shared by DS and Alzheimer's Disease (AD) indicate similar commonalities. This study aims to unravel the relationship between the canonical Wnt/pathway, the amyloid precursor protein processing, the telomere shortening in DS individuals.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is the most common cause of age-related dementia, and the presence of amyloid-β (Aβ) plaques and tau-containing neurofibrillary tangles is associated with the neurodegeneration and cognitive impairment in this incurable disease. Growing evidence shows that epigenetic dysregulation through histone deacetylases (HDACs) plays a critical role in synaptic dysfunction and memory loss in AD, and HDACs have been highlighted as a novel class of anti-Alzheimer targets. Moreover, restoring Wnt/β-catenin signaling, which is greatly suppressed in AD brains, is a promising therapeutic strategy for AD.
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