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RPS3 Aggravates Sepsis-Induced Acute Kidney Injury Through Activating NF-kappaB Mediated Renal Inflammatory

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  • 1Department of Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, China. zhangjun200504@163.com.

Physiological Research
|March 11, 2026
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Ribosomal protein S3 (RPS3) exacerbates sepsis-associated acute kidney injury (S-AKI) by activating the nuclear factor-kappa B (NF-kappaB) pathway. Targeting RPS3 may offer a new therapeutic strategy for S-AKI.

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Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Sepsis-associated acute kidney injury (S-AKI) is driven by excessive inflammation.
  • Nuclear factor-kappa B (NF-kappaB) signaling is crucial in S-AKI pathogenesis.
  • Ribosomal protein S3 (RPS3) is a known regulator of NF-kappaB, but its role in S-AKI is unclear.

Purpose of the Study:

  • To investigate the role of RPS3 in S-AKI-associated inflammation.
  • To elucidate the molecular mechanisms linking RPS3 to S-AKI.
  • To assess RPS3 as a potential therapeutic target for S-AKI.

Main Methods:

  • Analyzed urinary RPS3 and serum TNF-alpha in S-AKI patients.
  • Established a murine model of S-AKI using LPS injection.
  • Evaluated renal function, inflammation, RPS3 expression, and NF-kappaB activation in vivo.
  • Utilized RPS3 knockdown and NF-kappaB agonist in HK-2 cells to explore mechanisms.

Main Results:

  • Elevated urinary RPS3 and serum TNF-alpha in S-AKI patients, showing a positive correlation.
  • LPS-induced S-AKI mice exhibited impaired renal function, inflammation, increased RPS3, and NF-kappaB activation.
  • RPS3 knockdown in HK-2 cells reduced LPS-induced inflammation and NF-kappaB activation.
  • NF-kappaB agonist partially reversed the protective effects of RPS3 knockdown.

Conclusions:

  • RPS3 significantly contributes to the inflammatory response in S-AKI.
  • RPS3 activates the NF-kappaB signaling pathway in S-AKI.
  • RPS3 represents a promising therapeutic target for managing S-AKI.