What question did this study set out to answer?

This research aims to understand the role of heparanase in peritoneal fibrosis and its relationship with other fibrosis markers.

April 17, 2026

Exploring the Regulatory Role of Heparanase in Peritoneal Fibrosis via the HPA / SDC ‐1/ TGF ‐β Axis

Key Points

This research aims to understand the role of heparanase in peritoneal fibrosis and its relationship with other fibrosis markers.
Measured heparanase, syndecan-1, and fibrosis markers in peritoneal dialysate from ESRD patients.
Established a mouse model for peritoneal fibrosis with four treatment groups.
Utilized RT-qPCR and Western blot for tissue sample analysis of fibrosis markers.
Applied H&E and Masson staining to evaluate fibrosis in tissues.
HPA levels showed a positive correlation with syndecan-1, TGF-β, fibronectin, and collagen I.
HPA correlated positively with dialysis duration and high peritoneal transport function.
HPA inhibition reduced expression of key fibrosis markers and increased E-cadherin expression in mice.
Results were consistent with the effects seen in the Bailing treatment group.

Abstract

Peritoneal fibrosis (PF) is a serious complication in patients undergoing peritoneal dialysis (PD). Heparanase (HPA) may drive the progression of PF by promoting inflammation and tissue remodeling. This study aimed to evaluate HPA expression in peritoneal dialysate from end-stage renal disease (ESRD) patients receiving PD and to assess the correlation between HPA and fibrosis markers in PF. Peritoneal dialysate samples from ESRD patients were collected to measure HPA, syndecan-1 (SDC-1), and fibrosis markers. To further investigate the regulatory role of HPA in PF, a mouse model was established. Then mice were divided into four groups (n = 6 per group): control, PF, PF + HPSEi, and PF + Bailing groups. Tissue samples were collected for the detection of HPA, SDC-1, and fibrosis markers using RT-qPCR and Western blot. Fibrosis was evaluated via H&E and Masson staining. In peritoneal dialysate from 104 participants, HPA levels were positively correlated with SDC-1 (r = 0.617), TGF-β (r = 0.413), fibronectin (r = 0.278), and collagen I (r = 0.276). HPA (β = 0.0024), SDC-1 (β = 0.0572), TGF-β (β = 0.4358), and collagen I (β = 0.0023) were positively correlated with dialysis duration (all p < 0.05). Additionally, HPA was associated with high peritoneal transport function (p = 0.043). In mouse tissues, HPA inhibitor treatment downregulated TGF-β1, α-SMA, collagen I, and SDC-1, while upregulated E-cadherin expression and reducing tissue fibrosis. These effects were similar to those observed in the Bailing treatment group (all p < 0.05). HPA is positively correlated with SDC-1 and fibrosis markers. Inhibition of HPA attenuates PF, potentially through the HPA/SDC-1/TGF-β axis.

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