miR-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14

Guo, Yong; Liao, Yuanjiang

doi:10.1016/j.intimp.2017.09.002

Cited by 10 publications

(10 citation statements)

References 21 publications

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“…We obtained a total of 223 DEGs, and the upregulated genes were mainly enriched in inflammatory response, cell fibrosis, TNF signaling pathway, and MAPK signaling pathway. Previous studies have shown a significant association of IgAN development and prognosis with the inflammatory reaction [10, 11] and glomerular and tubular fibrosis [12, 13]. Tumor necrosis factor (TNF) is a critical cytokine involved in apoptosis, cell survival, inflammation, and immunity.…”

Section: Discussionmentioning

confidence: 99%

Screening and Bioinformatics Analysis of IgA Nephropathy Gene Based on GEO Databases

Wang

2019

BioMed Research International

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Purpose. To identify novel biomarkers of IgA nephropathy (IgAN) through bioinformatics analysis and elucidate the possible molecular mechanism. Methods. The GSE93798 and GSE73953 datasets containing microarray data from IgAN patients and healthy controls were downloaded from the GEO database and analyzed by the GEO2R web tool to obtain different expressed genes (DEGs). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI), and Biological Networks Gene Oncology tool (BiNGO) were then performed to elucidate the molecular mechanism of IgAN. Results. A total of 223 DEGs were identified, of which 21 were hub genes, and involved in inflammatory response, cellular response to lipopolysaccharide, transcription factor activity, extracellular exosome, TNF signaling pathway, and MAPK signaling pathway. Conclusions. TNF and MAPK pathways likely form the basis of IgAN progression, and JUN/JUNB, FOS, NR4A1/2, EGR1, and FOSL1/2 are novel prognostic biomarkers of IgAN.

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Section: Discussionmentioning

confidence: 99%

Screening and Bioinformatics Analysis of IgA Nephropathy Gene Based on GEO Databases

Wang

2019

BioMed Research International

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“…Systemic inflammatory events like sepsis may also increase circulating sTWEAK levels [87]. In this respect, some regulators of TWEAK with potential clinical interest have been identified: the microRNAs miR‐200bc/429 directly target TWEAK and are downregulated in human IgA nephropathy, and their overexpression in cultured podocytes and tubular cells decreased TWEAK and the inflammatory response [88].…”

Section: Tweak–fn14 and The Kidneymentioning

confidence: 99%

TWEAK–Fn14 as a common pathway in the heart and the kidneys in cardiorenal syndrome

et al. 2021

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There is a complex relationship between cardiac and renal disease, often referred to as the cardiorenal syndrome. Heart failure adversely affects kidney function, and both acute and chronic kidney disease are associated with structural and functional changes to the myocardium. The pathological mechanisms and contributing interactions that surround this relationship remain poorly understood, limiting the opportunities for therapeutic intervention. The cytokine tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor‐inducible 14 (Fn14), are abundantly expressed in injured kidneys and heart. The TWEAK–Fn14 axis promotes responses that drive tissue injury such as inflammation, proliferation, fibrosis, and apoptosis, while restraining the expression of tissue protective factors such as the anti‐aging factor Klotho and the master regulator of mitochondrial biogenesis peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α). High levels of TWEAK induce cardiac remodeling, and promote inflammation, tubular and podocyte injury and death, fibroblast proliferation, and, ultimately, renal fibrosis. Accordingly, targeting the TWEAK–Fn14 axis is protective in experimental kidney and heart disease. TWEAK has also emerged as a biomarker of kidney damage and cardiovascular outcomes and has been successfully targeted in clinical trials. In this review, we update our current knowledge of the roles of the TWEAK–Fn14 axis in cardiovascular and kidney disease and its potential contribution to the cardiorenal syndrome. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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“…In related experiments, Guo et al [53] found that the expression of the miR-200b,c/429 cluster was downregulated in IgAN kidney tissue, as well as in cultured podocytes generated from IgAN tissue and in HK-2 proximal tubular cells compared with matched controls. Overexpression of this miR cluster in IgAN-podocytes and HK-2 cells reduced the release of inflammatory cytokines MCP-1, IL-6 and RANTES.…”

Section: Kidney Tissue and Cultured Kidney Cellsmentioning

confidence: 98%

“…Overexpression of this miR cluster in IgAN-podocytes and HK-2 cells reduced the release of inflammatory cytokines MCP-1, IL-6 and RANTES. This is likely to have occurred as a result of miR-200b,c/429 targeting the 3'UTR region of TWEAK (TNF-like weak inducer of apoptosis), thereby inhibiting NF-KB pathway activation and supressing inflammation [53].…”

Section: Kidney Tissue and Cultured Kidney Cellsmentioning

confidence: 99%

“…As reviewed above, a number of miRs have been identified in kidney, urine and blood that have been reported as candidate biomarkers in IgAN. A number of these do fulfil some of the criteria listed above; they modulate relevant disease pathways (biologically plausible) [53,54], most are stable at room temperature [71], can be measured using accessible technology, RT-PCR [109], and are differentially expressed in the blood and urine of IgAN patients (minimally invasive). However, to date no single/panel of miR biomarkers has demonstrated generalisability across populations, or within a population across different sites.…”

Section: Mirs As Biomarkers In Iganmentioning

confidence: 99%

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The Non-Coding RNA Landscape in IgA Nephropathy—Where Are We in 2021?

Pawluczyk

Selvaskandan

Barratt

2021

JCM

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IgA nephropathy (IgAN) is the most commonly diagnosed primary glomerulonephritis worldwide. It is a slow progressing disease with approximately 30% of cases reaching end-stage kidney disease within 20 years of diagnosis. It is currently only diagnosed by an invasive biopsy and treatment options are limited. However, the current surge in interest in RNA interference is opening up new horizons for the use of this new technology in the field of IgAN management. A greater understanding of the fundamentals of RNA interference offers exciting possibilities both for biomarker discovery and, more importantly, for novel therapeutic approaches to target key pathogenic pathways in IgAN. This review aims to summarise the RNA interference literature in the context of microRNAs and their association with the multifaceted aspects of IgA nephropathy.

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miR-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14

Cited by 10 publications

References 21 publications

Screening and Bioinformatics Analysis of IgA Nephropathy Gene Based on GEO Databases

Screening and Bioinformatics Analysis of IgA Nephropathy Gene Based on GEO Databases

TWEAK–Fn14 as a common pathway in the heart and the kidneys in cardiorenal syndrome

The Non-Coding RNA Landscape in IgA Nephropathy—Where Are We in 2021?

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