更新于：2024-11-01

Peritoneal Fibrosis

腹膜纤维变性

更新于：2024-11-01

基本信息

别名

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

+ [23]

简介

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.

关联

项与腹膜纤维变性相关的药物

Alanylglutamine

丙氨酰谷氨酰胺

靶点

IL-17

作用机制

IL-17调节剂 [+1]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段批准上市

首次获批国家/地区

德国

首次获批日期1995-04-01

GYY-4137

靶点-

作用机制

H2S donor

在研机构

浙江大学

原研机构

National University of Singapore

在研适应症

腹膜纤维变性

非在研适应症

心血管疾病

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

Belnacasan

靶点

caspase 1

作用机制

caspase 1抑制剂

在研机构

Kawasaki Medical School

原研机构

Vertex Pharmaceuticals, Inc.

在研适应症

腹膜纤维变性

非在研适应症

癫痫部分性发作 [+2]

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与腹膜纤维变性相关的临床试验

ACTRN12624000831583 / Not yet recruitingN/AIIT

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

开始日期2024-08-01

申办/合作机构-

ChiCTR2300079292 / Suspended早期临床1期IIT

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

开始日期2024-01-01

申办/合作机构-

ChiCTR2300079318 / SuspendedN/AIIT

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

开始日期2024-01-01

申办/合作机构-

100 项与腹膜纤维变性相关的临床结果

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100 项与腹膜纤维变性相关的转化医学

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0 项与腹膜纤维变性相关的专利（医药）

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1,564

项与腹膜纤维变性相关的文献（医药）

2024-12-31·Renal Failure

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

Article

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

2024-12-31·Renal Failure

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

Article

作者: 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.

2024-12-31·Renal Failure

Pressure induces peritoneal fibrosis and inflammation through CD44 signaling

Article

作者: 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.

项与腹膜纤维变性相关的新闻（医药）

2023-07-25

·生物谷

专访中山大学彭晖｜发现腹膜纤维化产生新机制，设计AAV1基因疗法成功治疗小鼠模型

近日，中山大学附属第三医院彭晖教授团队通过对腹膜的单细胞转录组分析和细胞外囊泡的蛋白质组学分析，发现了导致腹膜纤维化的全新作用机制，为开发腹膜纤维化治疗策略提供了新思路。目前，这项研究已经以“Extr 发现腹膜纤维化潜在分子靶点并设计基因疗法成功治疗小鼠 “长期的腹膜透析容易导致腹膜纤维化，进而引起患者超滤功能障碍，甚至逐渐进展为超滤衰竭，为此，我们想探讨腹膜透析相关腹膜纤维化发生发展的机制，以找寻相关的治疗靶点。”彭晖介绍道。既往研究已经证实，腹膜细胞间的交流能够调控腹膜纤维化的发生。“作为细胞间交流的通讯介质，细胞外囊泡是当今的研究热点，其可以通过传递 DNA、RNA、蛋白质、脂质等生物活性分子调节靶细胞的生物学行为。所以，我们聚焦于细胞外囊泡在腹膜纤维化中的作用开展此次研究工作。”她说道。采用 AVV1 载体基因治疗腹膜纤维化未来有重要临床转化价值