ArticleScientific reports2022
ICAM-1 related long noncoding RNA is associated with progression of IgA nephropathy and fibrotic changes in proximal tubular cells.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Inflammation-related lncRNAs in the regulation of kidney injuries; special emphasis on novel lncRNA-based delivery platforms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Long non-coding RNA in IgA nephropathy: a comprehensive review.Renal failure · 2025Review
- LncRNAs and IgA nephropathy: underlying molecular pathways and clinical applications.Clinical and experimental medicine · 2025Review
- Beyond hemoglobin: Critical role of 2,3-bisphosphoglycerate mutase in kidney function and injury.Acta physiologica (Oxford, England) · 2025Article
- Prognostic value of serum complement cleavage factor Bb in idiopathic membranous nephropathy and establishment of nomogram model.Scientific reports · 2024Article
- Review
- Kidney Injury: Focus on Molecular Signaling Pathways.Current medicinal chemistry · 2024Review
- The Mission of Long Non-Coding RNAs in Human Adult Renal Stem/Progenitor Cells and Renal Diseases.Cells · 2023Review
- Serum Long Noncoding RNA H19 and CKD Progression in IgA Nephropathy.Journal of nephrology · 2023Article
- Urinary complement proteins in IgA nephropathy progression from a relative quantitative proteomic analysis.PeerJ · 2023Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intercellular adhesion molecule 1 (ICAM-1) related long noncoding RNA (ICR) is on the antisense strand of ICAM-1 and regulates ICAM-1 expression. ICAM-1 is involved in renal tubulointerstitial injury; however, the expression and clinical implication of ICR are not determined in IgA nephropathy (IgAN). We compared renal ICR levels in 337 IgAN patients with those of 89 biopsy controls, and a markedly increased ICR level was observed in IgAN patients. By Cox proportional hazards models, higher levels of renal ICR were independently associated with disease progression event defined as end-stage renal disease or ≥ 40% decline in estimated glomerular filtration rate. Patients in the highest tertile of renal ICR had a 3.5-fold higher risk for disease progression compared with those in the lowest tertile. The addition of renal ICR to a model with traditional risk factors improved risk prediction of disease progression (net reclassification index: 0.31 [95% CI 0.01-0.50]; integrated discrimination index: 0.10 [95% CI 0.04-0.16]). Inhibition of ICR by transfection with plasmids containing ICR shRNA significantly reduced expression of collagen I and α-SMA, and phosphorylation of Akt and mTOR in TGF-β1- treated HK-2 cells. Our findings suggest that renal ICR might be an independent predictor of IgAN progression and contribute to renal fibrosis.
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