ArticleJournal of bioenergetics and biomembranes2021
LINC00261 relieves the progression of sepsis-induced acute kidney injury by inhibiting NF-κB activation through targeting the miR-654-5p/SOCS3 axis.
Article in Journal of bioenergetics and biomembranes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury.Frontiers in immunology · 2026Review
- [LINC00261 suppresses esophageal squamous cell carcinoma proliferation, invasion, and metastasis by targeting the miR-23a-3p/ZNF292 axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Critical role of LncRNA in sepsis-associated acute kidney injury.Frontiers in pharmacology · 2025Review
- miR-654-5p Contributes to the Activation and Proliferation of Hepatic Stellate Cells by Targeting RXRα.Frontiers in cell and developmental biology · 2022Article
- An Update of Long-Noncoding RNAs in Acute Kidney Injury.Frontiers in physiology · 2022Review
- Non-Coding RNAs in Kidney Diseases: The Long and Short of Them.International journal of molecular sciences · 2021Review
- LINC00261: a burgeoning long noncoding RNA related to cancer.Cancer cell international · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening disease, which can cause the dysfunction of multiple organs, including kidney. Recently, a number of studies found that the long non-coding RNA (lncRNA) is closely associated with the development and progression of sepsis; however, the role of long intergenic non-protein coding RNA 261 (LINC00261) in sepsis-induced acute kidney injury is poorly understood. In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). In conclusion, our results demonstrate that LINC00261 may regulate the progression of sepsis-induced acute kidney injury via the miR-654-5p/SOCS3/NF-κB pathway and therefore provides a new insight into the treatment of this disease.
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Registered trials
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