Elevated levels of IL-6 in IgA nephropathy patients are induced by an epigenetically driven mechanism modulated by viral and bacterial RNA

Sallustio, Fabio; Picerno, Angela; Cimmarusti, Maria Teresa; Montenegro, Francesca; Curci, Claudia; Palma, Giuseppe De; Sivo, Carmen; Annese, Francesca; Fontò, Giulia; Stasi, Alessandra; Pesce, Francesco; Tafuri, Silvio; Leo, Vincenzo Di; Gesualdo, Loreto

doi:10.1016/j.ejim.2023.07.045

Cited by 4 publications

(4 citation statements)

References 37 publications

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“…This pathway is upregulated in patients with IgAN, resulting in elevated IL-6 levels. 28 Involvement of IL-6 plays a critical role in the IgA deposition process of IgAN. 29 PKR is typically activated by both viral and bacterial RNA species.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy

Gao,

Xu,

et al. 2024

Kidney International Reports

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Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy

Gao,

Xu,

et al. 2024

Kidney International Reports

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“…In support of this, the aforementioned connection to Parkinson’s disease cannot be detected in the cerebellum, where the bimodal methylation pattern cannot be observed [ 6 , 16 ]. Similarly, it would be interesting to see whether the associations between nc886 RNA levels and IgA nephropathy would remain significant after taking into account the stable regulators of the RNA levels [ 84 ]. A reanalysis with the methylation and genetic regulators included in the model would be warranted to confirm these results.…”

Section: Nc886 and Later-life Health Traitsmentioning

confidence: 99%

Non-coding 886 ( nc886 / vtRNA2-1 ), the epigenetic odd duck – implications for future studies

Raitoharju,

Rajić,

Marttila

2024

Epigenetics

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Non-coding 886 ( nc886 , vtRNA2–1 ) is the only human polymorphically imprinted gene, in which the methylation status is not determined by genetics. Existing literature regarding the establishment, stability and consequences of the methylation pattern, as well as the nature and function of the nc886 RNAs transcribed from the locus, are contradictory. For example, the methylation status of the locus has been reported to be stable through life and across somatic tissues, but also susceptible to environmental effects. The nature of the produced nc886 RNA(s) has been redefined multiple times, and in carcinogenesis, these RNAs have been reported to have conflicting roles. In addition, due to the bimodal methylation pattern of the nc886 locus, traditional genome-wide methylation analyses can lead to false-positive results, especially in smaller datasets. Herein, we aim to summarize the existing literature regarding nc886 , discuss how the characteristics of nc886 give rise to contradictory results, as well as to reinterpret, reanalyse and, where possible, replicate the results presented in the current literature. We also introduce novel findings on how the distribution of the nc886 methylation pattern is associated with the geographical origins of the population and describe the methylation changes in a large variety of human tumours. Through the example of this one peculiar genetic locus and RNA, we aim to highlight issues in the analysis of DNA methylation and non-coding RNAs in general and offer our suggestions for what should be taken into consideration in future analyses.

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“…After 48 h following the administration of imoxin, both CREB phosphorylation and IL-6 secretion were significantly reduced in IgA patients. [76] In this context, the use of imoxin reduces the levels of angiotensin II, pCREB, reactive oxygen species (ROS), and advanced glycosylation products (AGEs) in treated mice [77,78].…”

Section: A Promising Experimental Treatment: Imoxinmentioning

confidence: 99%

Refractory IgA Nephropathy: A Challenge for Future Nephrologists

Di Leo,

Annese,

Papadia

et al. 2024

Medicina

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IgA nephropathy (IgAN) represents the most prevalent form of primary glomerulonephritis, and, on a global scale, it ranks among the leading culprits behind end-stage kidney disease (ESKD). Presently, the primary strategy for managing IgAN revolves around optimizing blood pressure and mitigating proteinuria. This is achieved through the utilization of renin–angiotensin system (RAS) inhibitors, namely, angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs). As outlined by the KDIGO guidelines, individuals who continue to show a persistent high risk of progressive ESKD, even with comprehensive supportive care, are candidates for glucocorticoid therapy. Despite these therapies, some patients have a disease refractory to treatment, defined as individuals that present a 24 h urinary protein persistently >1 g after at least two rounds of regular steroids (methylprednisolone or prednisone) and/or immunosuppressant therapy (e.g., mycophenolate mofetil), or who do not tolerate regular steroids and/or immunosuppressant therapy. The aim of this Systematic Review is to revise the current literature, using the biomedical database PubMed, to investigate possible therapeutic strategies, including SGLT2 inhibitors, endothelin receptor blockers, targeted-release budesonide, B cell proliferation and differentiation inhibitors, fecal microbiota transplantation, as well as blockade of complement components.

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Elevated levels of IL-6 in IgA nephropathy patients are induced by an epigenetically driven mechanism modulated by viral and bacterial RNA

Cited by 4 publications

References 37 publications

Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy

Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy

Non-coding 886 ( nc886 / vtRNA2-1 ), the epigenetic odd duck – implications for future studies

Refractory IgA Nephropathy: A Challenge for Future Nephrologists

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