ArticleHuman mutation2026
Podoplanin Antibody SZ168 Alleviates Sepsis Inflammation and Macrophage Dysregulation via ERK Signaling.
Article in Human mutation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Podoplanin Antibody SZ168 Alleviates Sepsis Inflammation and Macrophage Dysregulation via ERK Signaling.Human mutation · 2026Article
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9 authors.
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Abstract
Background: Sepsis is a life-threatening condition marked by excessive inflammation and immune dysregulation. Macrophages are central to this process. Podoplanin (PDPN), a transmembrane glycoprotein, is upregulated in inflammatory macrophages, but its role in sepsis remains unclear. Objective: The aim of this study is to investigate the role of PDPN and the therapeutic potential of its monoclonal antibody SZ168 in LPS-induced macrophages and to extend these observations with supplementary in vivo and preliminary clinical validation. Methods: RAW264.7 macrophages were stimulated with LPS and treated with SZ168. PDPN expression and the effects of SZ168 on cytokine secretion, polarization, apoptosis, and ERK signaling were assessed by proteomics, qPCR, Western blotting, ELISA, and flow cytometry. siRNA-mediated PDPN knockdown was used to validate pathway dependence. During revision, additional Western blot validation of MEK, p90RSK, and c-Fos; supplementary in vivo experiments in a mouse sepsis model; and a preliminary clinical cohort analysis were incorporated to strengthen mechanistic and translational relevance. Results: LPS stimulation significantly upregulated PDPN expression at both mRNA and protein levels in macrophages. SZ168 treatment reduced LPS-induced secretion of IL-6, TNF- Conclusion: The PDPN monoclonal antibody SZ168 attenuates inflammatory responses, promotes anti-inflammatory macrophage polarization, and inhibits apoptosis through modulation of the ERK signaling pathway in LPS-induced macrophages. The supplementary in vivo and preliminary human data added during revision further support the translational relevance of PDPN as a therapeutic target in sepsis.
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