Investigation of the causal relationships between human IgG N-glycosylation and 12 common diseases associated with changes in the IgG N-glycome

Zaytseva, Olga O.; Sharapov, Sodbo; Perola, M.; Esko, Tõnu; Landini, Arianna; Hayward, Caroline; Wilson, James F.; Lauc, Gordan; Aulchenko, Yurii S.; Klarić, Lucija; Tsepilov, Yakov A.

doi:10.1093/hmg/ddab335

Cited by 12 publications

(8 citation statements)

References 87 publications

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“…Postoperative changes in protein glycosylation also appear to correlate with CPSP. Plasma protein glycosylation is a complex process which has interplay with specific SNPs already known to be associated with chronic pain states 65,66 . Trbojevic-Akmacic et al reported that plasma of chronic low back pain patients had an increase in high-branched N -glycan structures with concomitant decrease in high-mannose and glycans containing bisecting N -acetylglucosamine 67 .…”

Section: Other Epigenetic Changes To Putative Genesmentioning

confidence: 99%

“…Plasma protein glycosylation is a complex process which has interplay with specific SNPs already known to be associated with chronic pain states. 65,66 Trbojevic-Akmacic et al reported that plasma of chronic low back pain patients had an increase in high-branched N-glycan structures with concomitant decrease in high-mannose and glycans containing bisecting N-acetylglucosamine. 67 Similar, Freidin et al were able to demonstrate that changes in immunoglobulin G glycans that either promote or block antibody-dependent cell-mediated cytotoxicity were associated with chronic low back pain.…”

Section: Other Epigenetic Changes To Putative Genesmentioning

confidence: 99%

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Genetic risk factors for chronic postsurgical pain in children

Diatchenko

Ingelmo

2023

European Journal of Anaesthesiology

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Genetic risk factors for chronic postsurgical pain in adults have been established, but little is known whether the same associations exist in children. It is even less clear how much influence single nucleotide polymorphisms can exert on the phenotypic expression of chronic postsurgical pain in children in general. To this effect, a search was made for original articles which met the following criteria: evaluation of postsurgical pain in children with known genetic mutations or, conversely, evaluation of atypical pain trajectories of postsurgical children assessing for possible genetic mutations that may explain the phenotype. All titles and abstracts retrieved were reviewed for suitability for inclusion. The references of the selected articles were also checked for additional relevant papers. To assess the transparency and quality of the genetic studies both STrengthening the REporting of Genetic Association studies scores and Q-Genie scores were applied. Overall, there is a paucity of information regarding the link between genetic mutations and eventual chronic postsurgical pain development although there is some information on acute postoperative pain. Evidence has shown that the contribution of genetic risk factors to chronic postsurgical pain development appears to be minor, with its clinical relevance yet to be described. More advanced techniques in systems biology (proteomics, transcriptomics) suggest promising avenues for investigating the disease.

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Section: Other Epigenetic Changes To Putative Genesmentioning

confidence: 99%

Section: Other Epigenetic Changes To Putative Genesmentioning

confidence: 99%

Genetic risk factors for chronic postsurgical pain in children

Diatchenko

Ingelmo

2023

European Journal of Anaesthesiology

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“…Immunoglobulin G (IgG) glycosylation, which affects IgG binding affinity, was shown to correlate with chronological age by Gly-canAge (R = 0.76, MAE = 9.7)-remarkably, using information about the abundance of just three glycans [59]. Glycans have since been demonstrated to relate to obesity [61] and diseases of inflammation, cancer, and autoimmunity [60], which also lead to increased GlycanAge predictions.…”

Section: Exploring Relationships Beyond Epigeneticsmentioning

confidence: 99%

“…Beyond the protein concentrations themselves, the posttranslational modification of certain proteins by glycans has also been shown to track chronological age and certain physiological states [59][60][61]. Glycans are a diverse group of polysaccharide macromolecules that have varied biological roles, ranging from stabilizing other molecular structures to acting as ligands modulating protein-protein interactions [62].…”

Section: Exploring Relationships Beyond Epigeneticsmentioning

confidence: 99%

Epigenetic aging: Biological age prediction and informing a mechanistic theory of aging

Koch

Ideker

2022

J Intern Med

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Numerous studies have shown that epigenetic age-an individual's degree of aging based on patterns of DNA methylation-can be computed and is associated with an array of factors including diet, lifestyle, genetics, and disease. One can expect that still further associations will emerge with additional aging research, but to what end? Prediction of age was an important first step, butin our view-the focus must shift from chasing increasingly accurate age computations to understanding the links between the epigenome and the mechanisms and physiological changes of aging. Here, we outline emerging areas of epigenetic aging research that prioritize biological understanding and clinical application. First, we survey recent progress in epigenetic clocks, which are beginning to predict not only chronological age but aging outcomes such as all-cause mortality and onset of disease, or which integrate aging signals across multiple biological processes. Second, we discuss research that exemplifies how investigation of the epigenome is building a mechanistic theory of aging and informing clinical practice. Such examples include identifying methylation sites and the genes most strongly predictive of aging-a subset of which have shown strong potential as biomarkers of neurodegenerative disease and cancer; relating epigenetic clock predictions to hallmarks of aging; and using longitudinal studies of DNA methylation to characterize human disease, resulting in the discovery of epigenetic indications of type 1 diabetes and the propensity for psychotic experiences.

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“…These mechanisms encompass complement activation, Fcγ receptor binding, interaction with lectin receptors on antigen-presenting cells, and reactivity with autoantibodies [ 9 ]. Currently, many studies have been conducted on the causal relationship between IgG N-glycation and inflammatory and autoimmune diseases [ 21 , 22 , 23 ]. However, we have limited knowledge about the causal relationship between N-glycosylation of immunoglobulins and aging.…”

Section: Introductionmentioning

confidence: 99%

The Causality between Human Immunoglobulin G (IgG) N-Glycosylation and Aging: A Mendelian Randomization Study

Sun,

Jian,

Zhang

et al. 2024

Molecules

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Background: Immunoglobulin G (IgG) N-glycosylation is considered a potential biomarker for aging and various pathological conditions. However, whether these changes in IgG N-glycosylation are a consequence or a contributor to the aging process remains unclear. This study aims to investigate the causality between IgG N-glycosylation and aging using Mendelian randomization (MR) analysis. Methods: We utilized genetic variants associated with IgG N-glycosylation traits, the frailty index (FI), and leukocyte telomere length (LTL) from a previous genome-wide association study (GWAS) on individuals of European ancestry. Two-sample and multivariable MR analyses were conducted, employing the inverse-variance weighted (IVW) method. Sensitivity analyses were performed to assess potential confounding factors. Results: Using the IVW method, we found suggestive evidence of a causal association between GP14 and FI (β 0.026, 95% CI 0.003 to 0.050, p = 0.027) and LTL (β −0.020, 95% CI −0.037 to −0.002, p = 0.029) in the two-sample MR analysis. In the multivariable MR analysis, suggestive evidence was found for GP23 and FI (β −0.119, 95% CI −0.219 to −0.019, p = 0.019) and GP2 and LTL (β 0.140, 95% CI 0.020 to 0.260, p = 0.023). Conclusions: In conclusion, our results supported a potentially causal effect of lower GP23 levels on an advanced aging state. Additional verification is required to further substantiate the causal relationship between glycosylation and aging.

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Investigation of the causal relationships between human IgG N-glycosylation and 12 common diseases associated with changes in the IgG N-glycome

Cited by 12 publications

References 87 publications

Genetic risk factors for chronic postsurgical pain in children

Genetic risk factors for chronic postsurgical pain in children

Epigenetic aging: Biological age prediction and informing a mechanistic theory of aging

The Causality between Human Immunoglobulin G (IgG) N-Glycosylation and Aging: A Mendelian Randomization Study

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