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Standardized Colon Ascendens Stent Peritonitis in Rats - a Simple, Feasible Animal Model to Induce Septic Acute Kidney Injury
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NF-κB/miR-455-5p/SOCS3 Axis Aggravates Sepsis-Induced Acute Kidney Injury through Promoting Renal Inflammation.
Mingjuan Yan1,2, Ni Zhang3, Li Quan3
1Department of Nephrology, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, China, 384350173@qq.com.
Nephron
|October 8, 2024
Summary
Sepsis causes acute kidney injury (AKI) by upregulating miR-455-5p via NF-κB, worsening kidney damage. Inhibiting this pathway offers potential therapeutic strategies for septic AKI.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Sepsis is a primary cause of acute kidney injury (AKI), yet its pathogenesis remains incompletely understood.
- Effective diagnostic and therapeutic strategies for septic AKI are lacking due to its complex, multifactorial nature.
Purpose of the Study:
- To investigate the role of microRNA-455-5p (miR-455-5p) in the development of septic AKI.
- To elucidate the molecular mechanisms underlying miR-455-5p regulation and its downstream effects in septic AKI.
Main Methods:
- In vitro experiments using lipopolysaccharide (LPS)-stimulated mouse proximal tubular cells (BUMPT).
- In vivo studies involving LPS-induced sepsis in mice, with administration of miR-455-5p mimics or inhibitors.
- Analysis of NF-κB activation, miR-455-5p expression, SOCS3 levels, apoptosis, and kidney damage markers.
Main Results:
- LPS-induced sepsis significantly elevated miR-455-5p in renal tubular cells.
- NF-κB directly upregulates miR-455-5p, and its inhibition reduces miR-455-5p levels.
- miR-455-5p mimics exacerbated kidney damage and inflammation, while silencing miR-455-5p conferred protection.
- miR-455-5p targets SOCS3, with its expression inversely correlated to miR-455-5p levels.
Conclusions:
- An NF-κB/miR-455-5p/SOCS3 signaling axis contributes to kidney damage in septic AKI by promoting inflammation.
- Targeting this axis presents a potential therapeutic avenue for managing septic AKI.
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