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Molecular and Pathophysiological Mechanisms of Peritoneal Fibrosis in Peritoneal Dialysis
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Molecular and Pathophysiological Mechanisms of Peritoneal Fibrosis in Peritoneal Dialysis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 4701

Special Issue Editor

Dr. Kimio Watanabe

E-Mail Website
Guest Editor
University Hospital Blood Purification, Tohoku University, Sendai 980-8577, Japan
Interests: nephrology

Special Issue Information

Dear Colleagues,

Peritoneal dialysis (PD) is an efficient renal replacement therapy for patients with end-stage kidney disease. However, long-term PD causes peritoneal fibrosis accompanying morphologic and functional changes in the peritoneal membrane. Peritoneal fibrosis is one of the important causes of PD technique failure, but its molecular and pathophysiological mechanisms remain largely unclear. A number of studies demonstrated that TGF-β/Smad signaling is the key mediator associated with progressive peritoneal fibrosis. The high activation of this pathway increases the collagen deposition and thickening of the peritoneal membrane. The most well-known Smad-independent pathways include protein kinase C (PKC), the extracellular signal-regulated kinase (ERK), the c-Jun N-terminal kinase (JNK), and the phosphatidylinositol-3-kinase (PI3K). Accumulating evidence shows that TGF-β/Smad-dependent or -independent micro-RNAs can also regulate peritoneal fibrosis. Bioincompatible dialysis solution, which induces chronic peritoneal inflammation, is considered the main factor for peritoneal fibrosis. Continuous exposure to bioincompatible dialysis solution induces the mesothelial-to-mesenchymal transition (MMT) along with inflammation and angiogenesis. We take particular interest in original papers and reviews that report on the relevance of molecular and pathophysiological mechanisms involved in the pathogenesis of peritoneal fibrosis in PD.

Dr. Kimio Watanabe
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • peritoneal fibrosis
  • peritoneal dialysis
  • TGF-β/smad signaling
  • bioincompatible dialysis solution
  • peritoneal inflammation
  • mesothelial-to-mesenchymal transition

Published Papers (3 papers)

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Research

19 pages, 4005 KiB  
Article
High Salt Promotes Inflammatory and Fibrotic Response in Peritoneal Cells
by Domonkos Pap, Csenge Pajtók, Apor Veres-Székely, Beáta Szebeni, Csenge Szász, Péter Bokrossy, Réka Zrufkó, Ádám Vannay, Tivadar Tulassay and Attila J. Szabó
Int. J. Mol. Sci. 2023, 24(18), 13765; https://doi.org/10.3390/ijms241813765 - 06 Sep 2023
Viewed by 1218
Abstract
Recent studies draw attention to how excessive salt (NaCl) intake induces fibrotic alterations in the peritoneum through sodium accumulation and osmotic events. The aim of our study was to better understand the underlying mechanisms. The effects of additional NaCl were investigated on human [...] Read more.
Recent studies draw attention to how excessive salt (NaCl) intake induces fibrotic alterations in the peritoneum through sodium accumulation and osmotic events. The aim of our study was to better understand the underlying mechanisms. The effects of additional NaCl were investigated on human primary mesothelial cells (HPMC), human primary peritoneal fibroblasts (HPF), endothelial cells (HUVEC), immune cells (PBMC), as well as ex vivo on peritoneal tissue samples. Our results showed that a high-salt environment and the consequently increased osmolarity increase the production of inflammatory cytokines, profibrotic growth factors, and components of the renin–angiotensin–aldosterone system, including IL1B, IL6, MCP1, TGFB1, PDGFB, CTGF, Renin and Ace both in vitro and ex vivo. We also demonstrated that high salt induces mesenchymal transition by decreasing the expression of epithelial marker CDH1 and increasing the expression of mesenchymal marker ACTA2 and SNAIL1 in HPMCs, HUVECs and peritoneal samples. Furthermore, high salt increased extracellular matrix production in HPFs. We demonstrated that excess Na+ and the consequently increased osmolarity induce a comprehensive profibrotic response in the peritoneal cells, thereby facilitating the development of peritoneal fibrosis. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Mechanisms of Peritoneal Fibrosis in Peritoneal Dialysis)
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16 pages, 4678 KiB  
Article
Peritoneal Expression of Membrane Complement Regulators Is Decreased in Peritoneal Dialysis Patients with Infected Peritonitis
by Sosuke Fukui, Masashi Mizuno, Mitsuhiro Tawada, Yasuhiro Suzuki, Hiroshi Kojima, Yoshihisa Matsukawa, Masaki Imai, Hangsoo Kim, Hiroshi Kinashi, Makoto Mizutani, Kenichi Minoshima, Shoichi Maruyama and Yasuhiko Ito
Int. J. Mol. Sci. 2023, 24(11), 9146; https://doi.org/10.3390/ijms24119146 - 23 May 2023
Viewed by 1186
Abstract
In peritoneal dialysis (PD) patients, fungi and Pseudomonas aeruginosa are considered important causative microorganisms for peritonitis with poor prognosis. Our objective was to explore expressions of membrane complement (C) regulators (CRegs) and tissue injuries in the peritoneum of patients with PD-related peritonitis, including [...] Read more.
In peritoneal dialysis (PD) patients, fungi and Pseudomonas aeruginosa are considered important causative microorganisms for peritonitis with poor prognosis. Our objective was to explore expressions of membrane complement (C) regulators (CRegs) and tissue injuries in the peritoneum of patients with PD-related peritonitis, including fungal and Pseudomonas aeruginosa peritonitis. In peritoneal biopsy tissues obtained at PD catheter removal, we investigated the severity of peritonitis-associated peritoneal injuries and the expression of CRegs, CD46, CD55, and CD59 against peritoneal tissues without any episode of peritonitis. In addition, we evaluated peritoneal injuries among fungal and Pseudomonas aeruginosa-peritonitis (P1) and Gram-positive bacterial peritonitis (P2). We also observed deposition of C activation products such as activated C and C5b-9 and measured sC5b-9 in the PD fluid of patients. As a result, the severity of peritoneal injuries correlated inversely with the expression of peritoneal CRegs. Peritoneal CReg expression in peritonitis was significantly reduced compared to no peritonitis. Peritoneal injuries were more severe in P1 than in P2. CReg expression was further decreased and C5b-9 further increased in P1 than in P2. In conclusion, severe peritoneal injuries due to fungal and Pseudomonas aeruginosa-peritonitis decreased CReg expression and increased deposition of activated C3 and C5b-9 in the peritoneum, suggesting that peritonitis, particularly fungal and Pseudomonas aeruginosa-peritonitis, might induce susceptibility to further peritoneal injuries due to excessive C activation. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Mechanisms of Peritoneal Fibrosis in Peritoneal Dialysis)
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13 pages, 2420 KiB  
Article
The Transfer of the Hepatocyte Growth Factor Gene by Macrophages Ameliorates the Progression of Peritoneal Fibrosis in Mice
by Yoko Obata, Katsushige Abe, Masanobu Miyazaki, Takehiko Koji, Yasuhiko Tabata and Tomoya Nishino
Int. J. Mol. Sci. 2023, 24(8), 6951; https://doi.org/10.3390/ijms24086951 - 09 Apr 2023
Cited by 1 | Viewed by 1491
Abstract
Growing evidence indicates that hepatocyte growth factor (HGF) possesses potent antifibrotic activity. Furthermore, macrophages migrate to inflamed sites and have been linked to the progression of fibrosis. In this study, we utilized macrophages as vehicles to express and deliver the HGF gene and [...] Read more.
Growing evidence indicates that hepatocyte growth factor (HGF) possesses potent antifibrotic activity. Furthermore, macrophages migrate to inflamed sites and have been linked to the progression of fibrosis. In this study, we utilized macrophages as vehicles to express and deliver the HGF gene and investigated whether macrophages carrying the HGF expression vector (HGF-M) could suppress peritoneal fibrosis development in mice. We obtained macrophages from the peritoneal cavity of mice stimulated with 3% thioglycollate and used cationized gelatin microspheres (CGMs) to produce HGF expression vector-gelatin complexes. Macrophages phagocytosed these CGMs, and gene transfer into macrophages was confirmed in vitro. Peritoneal fibrosis was induced by intraperitoneal injection of chlorhexidine gluconate (CG) for three weeks; seven days after the first CG injection, HGF-M was administered intravenously. Transplantation of HGF-M significantly suppressed submesothelial thickening and reduced type III collagen expression. Moreover, in the HGF-M-treated group, the number of α-smooth muscle actin- and TGF-β-positive cells were significantly lower in the peritoneum, and ultrafiltration was preserved. Our results indicated that the transplantation of HGF-M prevented the progression of peritoneal fibrosis and indicated that this novel gene therapy using macrophages may have potential for treating peritoneal fibrosis. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Mechanisms of Peritoneal Fibrosis in Peritoneal Dialysis)
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