Last update 01 Nov 2024

Peritoneal Fibrosis

Last update 01 Nov 2024

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.

VUmc [+2]

Originator Org.

Fresenius Kabi AG

Active Indication

Glutamine Deficiency, Congenital [+2]

Inactive Indication

Dietary Supplement [+1]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date01 Apr 1995

GYY-4137

Target-

Mechanism

H2S donor

Active Org.

Zhejiang University

Originator Org.

National University of Singapore

Active Indication

Peritoneal Fibrosis

Inactive Indication

Cardiovascular Diseases

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Belnacasan

Target

caspase 1

Mechanism

caspase 1 inhibitors

Active Org.

Kawasaki Medical School

Originator Org.

Vertex Pharmaceuticals, Inc.

Active Indication

Peritoneal Fibrosis

Inactive Indication

Epilepsies, Partial [+2]

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

1,564

Literatures (Medical) associated with Peritoneal Fibrosis

31 Dec 2024·Renal Failure

The role of computed tomography in the diagnosis of encapsulating peritoneal sclerosis in patients undergoing peritoneal dialysis

Article

Author: Li, Aomei ; Zhou, Dan ; Lin, Hongli ; Guo, Fujia ; Cui, Wengting ; Li, Longkai ; Li, Lin ; Yang, Wei ; Wu, Shuran ; Yu, Changqing

31 Dec 2024·Renal Failure

MiR-454-3p regulates high glucose-induced mesothelial-mesenchymal transition and glycolysis in peritoneal mesothelial cells by targeting STAT3

Article

Author: Shao, Xiaoqi ; Wang, Qiufeng ; Zhang, Pei ; Yao, Ling ; Fu, Jiao ; Li, Nan ; Rao, Qingqing

BACKGROUNDThe quality of life of patients receiving long-term peritoneal dialysis (PD) is significantly impacted by the onset of peritoneal fibrosis (PF), and one of the pathological changes is mesothelial-mesenchymal transition (MMT). In this study, we investigated the potential roles of miR-454-3p and signal transducer and activator of transcription 3 (STAT3) in the progression of peritoneal MMT and the underlying mechanisms.METHODSPeritoneums were collected to detect morphology via hematoxylin-eosin staining and differentially expressed miRNAs were detected via RT-qPCR. PD effluent-derived cell populations in the peritoneal cavity were isolated from the effluents of 20 PD patients to determine miR-454-3p, STAT3, and MMT markers via Western blotting and RT-qPCR. The relationship between miR-454-3p and STAT3 was examined via a dual-luciferase reporter assay. Western blotting and RT-qPCR were utilized to evaluate the expression of STAT3, MMT markers, and glycolytic enzymes. Immunofluorescence staining revealed the localization and expression of MMT markers and STAT3.RESULTSMiR-454-3p was downregulated in the peritoneums and PD effluent-derived cell populations of long-term PD patients. High glucose (HG) treatment promoted HMrSV5 cell MMT and glycolysis. MiR-454-3p overexpression alleviated HG-induced MMT and suppressed the expression of STAT3 and glycolytic enzymes. In contrast, the miR-454-3p inhibitor exacerbated HG-induced MMT and promoted the expression of glycolytic enzymes and STAT3. Moreover, STAT3 was the target of miR-454-3p.CONCLUSIONSThis study demonstrated the protective role of miR-454-3p in HG-induced MMT and glycolysis in HMrSv5 cells, suggesting that miR-454-3p may prevent MMT by suppressing glycolytic enzymes via the STAT3/PFKFB3 pathway in the HG environment.

31 Dec 2024·Renal Failure

Pressure induces peritoneal fibrosis and inflammation through CD44 signaling

Article

Author: Cherng, Yih-Giun ; Hsu, Yung-Ho ; Wu, Mei-Yi ; Wu, Mai-Szu ; Chen, Cheng-Hsien ; Huang, Nai-Jen ; Liao, Chia-Te ; Chen, Yu-Wei

Peritoneal dialysis (PD) is a widely used sustainable kidney replacement therapy. Prolonged use of PD fluids is associated with mesothelial-mesenchymal transition, peritoneal fibrosis, and eventual ultrafiltration (UF) failure. However, the impact of pressure on the peritoneum remains unclear. In the present study, we hypothesized increased pressure is a potential contributing factor to peritoneal fibrosis and investigated the possible mechanisms. In vitro experiments found that pressurization led to a mesenchymal phenotype, the expression of fibrotic markers and inflammatory factors in human mesothelial MeT-5A cells. Pressure also increased cell proliferation and augmented cell migration potential in MeT-5A cells. The mouse PD model and human peritoneum equilibrium test (PET) data both showed a positive association between higher pressure and increased small solute transport, along with decreased net UF. Mechanistically, we found that significant upregulation of CD44 in mesothelial cells upon pressurization. Notably, the treatment of CD44 neutralizing antibodies prevented pressure-induced phenotypic changes in mesothelial cells, while a CD44 inhibitor oligo-fucoidan ameliorated pressure-induced peritoneal thickening, fibrosis, and inflammation in PD mice. To conclude, intraperitoneal pressure results in peritoneal fibrosis in PD via CD44-mediated mesothelial changes and inflammation. CD44 blockage can be utilized as a novel preventive approach for PD-related peritoneal fibrosis and UF failure.

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Peritoneal Fibrosis

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