ReviewFrontiers in pharmacology2025
Critical role of LncRNA in sepsis-associated acute kidney injury.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- The LINC00920/miR-6834-3p/CPN1 Axis Modulates Immune Dysregulation in Sepsis-Associated Acute Kidney Injury and Serves as a Diagnostic Biomarker.Biochemical genetics · 2026Article
- Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is defined as organ dysfunction resulting from a harmful host response to infection. It can lead to multiple organ dysfunction, with the kidneys being one of the most commonly affected organs, resulting in sepsis-associated acute kidney injury (SA-AKI), which is associated with a high mortality rate. Despite significant advances in the treatment of SA-AKI in recent years, the condition continues to exhibit a high mortality rate. It remains a critical issue and clinical burden that necessitates further research to mitigate both acute and chronic consequences. An in-depth exploration of the pathogenesis of SA-AKI is essential for guiding early diagnosis and treatment. Increasing evidence indicates that long non-coding RNAs (LncRNAs) play a crucial role in SA-AKI, typically functioning as competing endogenous RNAs (ceRNAs) that alleviate the inhibition of downstream target genes by microRNAs (miRNAs), thus regulating downstream signaling pathways and participating in vital cellular biological processes and inflammatory responses. A growing number of studies have reported the involvement of LncRNAs in SA-AKI, highlighting the necessity of summarizing the evidence on this topic through a comprehensive review, as LncRNAs can either promote the onset or inhibit the progression of SA-AKI depending on the underlying mechanisms. This paper reviews the pathophysiological mechanisms contributing to the development of SA-AKI, the pivotal role of LncRNAs in this condition, and their potential as biomarkers and therapeutic targets, aiming to provide theoretical guidance for the study and treatment of SA-AKI.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.