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Research Snapshot Theater: Veterinarian

USP5 Inhibition Attenuates Sepsis-Induced Liver Injury via Downregulation of the TXNIP/NLRP3 Pathway

Sunday, March 22, 2026
2:30 PM - 3:30 PM Central Time
Location: Connections Central - RST 12

  • Songchang Shi, MD, PhD (he/him/his)

    Fujian, CHN

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • LZ

    Lihui Zhang, MD

    Critical Care Physician
    Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, China (People's Republic)

    Disclosure information not submitted.

  • XP

    Xiaobin Pan, MD

    Critical Care Physician
    Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, China (People's Republic)

    Disclosure information not submitted.

  • SZ

    Shujuan Zhang, MD

    Critical Care Physician
    Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, China (People's Republic)

    Disclosure information not submitted.

  • WL

    Wei Lin, MD, PhD

    ndocrinologist, Visiting Scholar at Brigham and Women’s Hospital
    Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, Brigham and Women’s Hospital, China (People's Republic)

    Disclosure information not submitted.

Introduction: Sepsis is a systemic inflammatory response that frequently results in multiple organ dysfunction, including significant liver injury. Ubiquitin-specific protease 5 (USP5) has been shown to stabilize thioredoxin-interacting protein (TXNIP), thereby promoting inflammatory signaling in hepatocytes. However, the in vivo relevance of this mechanism in sepsis-related liver injury remains unclear.


Methods: A cellular model of sepsis was established using lipopolysaccharide (LPS) to stimulate HepG2 and Huh7 cells. A murine sepsis model was created via cecal ligation and puncture (CLP). The USP5 inhibitor USP5-IN-1 was administered to both LPS-stimulated cells and CLP mice. Protein and mRNA levels of TXNIP and pyroptosis-related markers (NLRP3, ASC, cleaved caspase-1) were assessed using Western blot and qPCR. IL-1β and IL-18 levels were measured by ELISA and qPCR. Cell viability and proliferation were assessed using CCK-8 and Ki-67 immunostaining; apoptosis was evaluated using Annexin V/PI staining and TUNEL assay. Histologic liver injury was assessed via H&E staining.


Results: USP5-IN-1 treatment significantly reduced TXNIP expression and downstream NLRP3 inflammasome activation in LPS-induced hepatocytes, without affecting baseline USP5 expression. Levels of IL-1β and IL-18 were also significantly decreased. USP5-IN-1 improved cell viability, reduced apoptosis, and promoted proliferation. In CLP mice, USP5 inhibition alleviated liver injury, reduced serum proinflammatory cytokines, and downregulated TXNIP/NLRP3 pathway activation.


Conclusions: USP5 inhibition protects against sepsis-induced liver injury through suppression of the TXNIP/NLRP3 inflammasome pathway. These findings suggest that USP5 may represent a novel therapeutic target for managing hepatic dysfunction in septic patients.