ArticleThe Kaohsiung journal of medical sciences2024
Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury.
Article in The Kaohsiung journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- Review
- MALAT1 promotes acetaminophen-induced hepatocyte pyroptosis by stabilizing Rac1 through its interaction with MTDH and the hepatoprotective role of muniziqi saifula.Molecular and cellular biochemistry · 2026Article
- The possible role of astaxanthin in cisplatin-induced nephrotoxicity in rats: interplay between non-coding RNA, redox state, inflammation, and ferroptosis: a histological, immunohistochemical, and biochemical study.Journal of molecular histology · 2026Article
- Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury.Frontiers in immunology · 2026Review
- Single-cell transcriptomics identifies ergothioneine as a mitochondrial protector to prevent AKI-to-CKD progression.PloS one · 2026Article
- Critical role of LncRNA in sepsis-associated acute kidney injury.Frontiers in pharmacology · 2025Review
- Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury.The Kaohsiung journal of medical sciences · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
Septic acute kidney injury (AKI) is a fatal disease in the intensive care unit, with ferroptosis playing a crucial role in its pathogenesis. Long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in septic-induced AKI inflammation and apoptosis. However, its regulatory role in ferroptosis and underlying mechanisms remain unclear. In vivo and in vitro models of septic AKI were established using cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) challenge, respectively. Serum levels of creatinine (Cr), blood urea nitrogen (BUN), kidney injury molecule-1 (Kim-1), neutrophil gelatinase-associated lipocalin (NGAL), and inflammatory cytokine in kidney tissues were determined by ELISA kits. Histopathological alterations and apoptosis were evaluated by HE staining and TUNEL. Ferroptosis was accessed by measuring MDA, GSH, Fe
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