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Last update 08 May 2025

Peritoneal Fibrosis

Last update 08 May 2025

Basic Info

Synonyms

Fibroses, Peritoneal, Fibrosing Syndrome, Peritoneal, Fibrosing Syndromes, Peritoneal

+ [23]

Introduction

Disorder characterized by a wide range of structural changes in PERITONEUM, resulting from fibrogenic or inflammatory processes. Peritoneal fibrosis is a common complication in patients receiving PERITONEAL DIALYSIS and contributes to its gradual decrease in efficiency.

Drugs associated with Peritoneal Fibrosis

Alanylglutamine

Target

IL-17

Mechanism

IL-17 modulators [+1]

Active Org.

Fresenius SE & Co. KGaA [+2]

Originator Org.

Fresenius Kabi AG

Active Indication

Glutamine Deficiency, Congenital [+2]

Inactive Indication

Dietary Supplement [+2]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

Germany

First Approval Date01 Apr 1995

GPCR antagonist(Viva Star)

Target

GPCR

Mechanism

GPCR antagonists

Active Org.

Viva Star Biosciences (Suzhou) Co., Ltd.

Originator Org.

Viva Star Biosciences (Suzhou) Co., Ltd.

Active Indication

Fibrosis [+5]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

GYY-4137

Target-

Mechanism

H2S donor

Active Org.

Shanghai Changzheng Hospital [+2]

Originator Org.

National University of Singapore

Active Indication

Osteoarthritis [+1]

Inactive Indication

Cardiovascular Diseases

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Peritoneal Fibrosis

ACTRN12624000831583

/ Not yet recruitingNot ApplicableIIT

Indocyanine green for ureteric identification in complex gynaecology surgery: A single centered, randomised, double-blinded feasibility study in women planned to undergo complex gynaecological laparoscopic surgery

Start Date01 Aug 2024

Sponsor / Collaborator-

ChiCTR2300079292

/ SuspendedEarly Phase 1IIT

Expression of protein methyltransferase, deacetylase, deubiquitination enzyme, GPD2, pyrodeath and autophagy related proteins in human peritoneal tissue and peritoneal effluents

Start Date01 Jan 2024

Sponsor / Collaborator-

ChiCTR2300079318

/ SuspendedNot ApplicableIIT

Clinical study on early diagnosis and progression monitoring of peritoneal fibrosis using FAPI-PET imaging

Start Date01 Jan 2024

Sponsor / Collaborator-

100 Clinical Results associated with Peritoneal Fibrosis

100 Translational Medicine associated with Peritoneal Fibrosis

0 Patents (Medical) associated with Peritoneal Fibrosis

1,410

Literatures (Medical) associated with Peritoneal Fibrosis

31 Dec 2025·Renal Failure

Role of macrophages in peritoneal dialysis-associated peritoneal fibrosis

Review

Author: Chu, Chenling ; Cao, Luxi ; Huang, Ying ; Zhu, Bin ; Shen, Quanquan ; Ji, Shuiyu

Peritoneal dialysis (PD) can be used as renal replacement therapy when chronic kidney disease (CKD) progresses to end-stage renal disease. However, peritoneal fibrosis (PF) is a major cause of PD failure. Studies have demonstrated that PD fluid contains a significantly larger numbers of macrophages compared with the healthy individuals. During PD, macrophages can secrete cytokines to keep peritoneal tissue in sustained low-grade inflammation, and participate in the regulation of fibrosis-related signaling pathways, such as NF-κB, TGF-β/Smad, IL4/STAT6, and PI3K/AKT. A series of basic pathological changes occurs in peritoneal tissues, including epithelial mesenchymal transformation, overgeneration of neovasculature, and abnormal deposition of extracellular matrix. This review focuses on the role of macrophages in promoting PF during PD, summarizes the targets of macrophage-related inhibition of fibrosis, and provides new ideas for clinical research on delaying PF, maintaining the function and integrity of peritoneum, prolonging duration of PD as a renal replacement modality, and achieving longer survival in CKD patients.

30 Apr 2025·The FASEB Journal

Targeting MLL1/WDR5‐Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16^INK4a

Article

Author: Osaki, Yosuke ; Maeda, Kazuya ; Hara, Daisuke ; Nakashima, Ayumu ; Masaki, Takao ; Doi, Shigehiro ; Ishiuchi, Naoki ; Ike, Takeshi ; Takahashi, Akira ; Chiba, Takuto ; Maeoka, Yujiro ; Yoshida, Maria ; Doi, Toshiki ; Sasaki, Kensuke

ABSTRACTPeritoneal fibrosis poses a significant challenge to the long‐term efficacy of peritoneal dialysis (PD), with emerging evidence highlighting the role of cellular senescence in its pathogenesis. p16INK4a is a cell cycle regulator that has been implicated in cellular senescence. Mixed‐lineage leukemia 1 (MLL1) forms a complex with WD‐40 repeat protein 5 (WDR5) and exhibits histone H3K4 methyltransferase activity. We have previously shown that inhibition of the MLL1/WDR5 complex reduces p16INK4a expression and attenuates renal senescence after injury in mice. This study aimed to investigate whether inhibiting MLL1/WDR5 attenuates peritoneal senescence, inflammation, and fibrosis in both human samples and in mice with methylglyoxal (MGO)‐induced peritoneal fibrosis (MGO‐injected mice), while also exploring the associated underlying mechanisms. MLL1/WDR5, histone 3 lysine 4 trimethylation (H3K4me3), and p16INK4a expression were elevated in TGF‐β1‐stimulated human peritoneal mesothelial cells (HPMCs), non‐adherent cells obtained from patients undergoing PD, and the submesothelial compact zones of MGO‐injected mice. Notably, p16INK4a expression in these cells was positively correlated with the dialysate/plasma creatinine ratio. Treatment with the MLL1/WDR5 protein–protein interaction inhibitors MM‐102 and OICR‐9429 reduced H3K4me3 levels and p16INK4a expression, suppressing fibrosis in HPMCs as well as peritoneal fibrosis and inflammation in MGO‐injected mice. These inhibitors also improved peritoneal function in MGO‐injected mice. Additionally, we demonstrated that MLL1/WDR5‐induced H3K4me3 directly regulates p16INK4a gene transcription, and that inhibiting MLL1/WDR5 reduces H3K4me3, thereby suppressing p16INK4a gene transcription. These findings suggest that targeting MLL1/WDR5 activation alleviates peritoneal senescence, inflammation, and fibrosis, highlighting its potential as a promising therapeutic strategy for peritoneal fibrosis.

01 Apr 2025·Small

Inhibition of Caspase‐1 Suppresses GSDMD‐mediated Peritoneal Mesothelial Cell Pyroptosis and Inflammation in Peritoneal Fibrosis

Article

Author: Liu, Na ; Shi, Yingfeng ; Hu, Yan ; Zhuang, Shougang ; Chen, Hui ; Zhong, Qin ; Ma, Xiaoyan ; Zhang, Shasha ; Li, Jinqing ; Li, Xialin

AbstractPyroptosis, belonging to programmed cell death, is shown to be mediated by gasdermin D (GSDMD) and gains more and more attention in innate immunity and multiple diseases. However, the role of GSDMD‐mediated pyroptosis in peritoneal fibrosis (PF) remains unclear. This study observed NLRP3 inflammasome activation and pyroptosis in the peritoneum of long‐term peritoneal dialysis (PD) patients with PF. Moreover, it is found that high glucose (HG) can induce the activation of NLRP3 inflammasome by regulating TLR4/NF‐κB and JNK/p38 MAPK signaling in human peritoneal mesothelial cells (HPMCs), leading to subsequent Caspase‐1 activation. The cleaved Caspase‐1 promoted pyroptosis‐related transmembrane pore formation through activating GSDMD‐N, and stimulated the HPMCs to secrete inflammatory factors including IL‐1β and IL‐18. GSDMD global deletion or pharmacologic pretreatment with Caspase‐1 specific inhibitor VX‐765 effectively inhibited the pyroptosis and inflammation, thereby ameliorating PF. Additionally, treatment with VX‐765 and transfected with Caspase‐1 siRNA or GSDMD siRNA also inhibited the transmembrane pore formation and inflammatory factors secretion in HG‐induced HPMCs. Consistent with these results, delayed treatment with VX‐765 also alleviated PF, indicating the therapeutic effect of VX‐765. Taken together, the results demonstrate that pyroptosis may be a novel therapeutic target for peritoneal fibrosis.

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