ArticleBioengineered2022
MicroRNA-103a-3p enhances sepsis-induced acute kidney injury via targeting CXCL12.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Identification and functional validation of mitochondria-related genes associated with tubular injury in kidney transplantation and ischemia-reperfusion injury.Biology direct · 2026Article
- Sepsis-Associated Acute Kidney Injury: What's New Regarding Its Diagnostics and Therapeutics?Diagnostics (Basel, Switzerland) · 2024Review
- miR-16-5p aggravates sepsis-associated acute kidney injury by inducing apoptosis.Renal failure · 2024Article
- Kidney Injury: Focus on Molecular Signaling Pathways.Current medicinal chemistry · 2024Review
- Vancomycin Induced Ferroptosis in Renal Injury Through the Inactivation of Recombinant Glutathione Peroxidase 4 and the Accumulation of Peroxides.Drug design, development and therapy · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a common and fatal complication in inflammatory sepsis. Several microRNAs (miRNAs or miRs) have been identified to control sepsis. MiR-103a-3p has been reported to take part in the various inflammatory response. However, its role in AKI remains unclear. The present research aimed to explore the role and mechanisms of miR-103a-3p in AKI. Neurogenic sepsis mouse model and lipopolysaccharide-induced HK-2 and 293 cell models were established. The renal functions in each group of mice were measured. After evaluating the biological functions of C-X-C motif chemokine 12 (CXCL12) and miR-103a-3p on HK-2 and HEK-293 T cells, their interaction was determined. Detection of CXCL12 and apoptosis and inflammation-related factors in renal tissue was done. MiR-103a-3p was significantly repressed in the sepsis model, while CXCL12 was elevated. Furthermore, miR-103a-3p inversely controlled CXCL12. Knockdown of miR-103a-3p or overexpression of CXCL12 could significantly inhibit the progression of HK-2 and HEK293 cells, whereas elevated miR-103a-3p or knockdown of CXCL12 showed the opposite effects. Collectively, miR-103a-3p heightens renal cell damage caused by sepsis by targeting CXCL12.
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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.