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Cells
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Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms
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Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 6088

Special Issue Editor

Dr. Zhuo Wang

E-Mail Website
Guest Editor
School of Life and Health Sciences, Aston University, Birmingham, UK
Interests: fibrotic diseases; cancer; pathological angiogenesis

Special Issue Information

Dear Colleagues,

This Special Issue of Cells is dedicated to the molecular signals and cellular mechanisms of organ and tissue fibrosis. Fibrosis is characterized as the formation and remodelling of scar tissue and is an end result of many conditions, such as injury and inflammation. Fibrosis leads to the loss of tissue and organ functions, while fibrotic disorders contribute to around 40% of all causes of mortality. Even though fibrosis occurs in the extracellular matrix, understanding the role of cells and molecular signals in organ fibrosis is important to enhance our knowledge of this pathological process and eventually develop effective treatments. This Special Issue will focus on various cellular and molecular mechanisms during fibrosis in various organs, such as inflammatory cytokine-induced cell transition into myofibroblasts. This Special Issue will contain both original research articles and reviews. Studies performed using in vitro, ex vivo and in vivo models are welcome.

Dr. Zhuo Wang
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • fibrosis
  • scarring
  • cytokine
  • myofibroblasts
  • extracellular matrix
  • growth factors
  • mesenchymal transition

Published Papers (4 papers)

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Research

11 pages, 2987 KiB  
Communication
Lung Cancers: Parenchymal Biochemistry and Mechanics
by Yves Lecarpentier, Bruno Tremblay, Christèle Locher, Olivier Schussler, Alexandre Vallée, Christophe Locher and David Pho
Cells 2024, 13(5), 427; https://doi.org/10.3390/cells13050427 - 29 Feb 2024
Viewed by 664
Abstract
Parenchyma of pulmonary cancers acquires contractile properties that resemble those of muscles but presents some particularities. These non-muscle contractile tissues could be stimulated either electrically or chemically (KCl). They present the Frank–Starling mechanism, the Hill hyperbolic tension–velocity relationship, and the tridimensional time-independent tension–velocity–length [...] Read more.
Parenchyma of pulmonary cancers acquires contractile properties that resemble those of muscles but presents some particularities. These non-muscle contractile tissues could be stimulated either electrically or chemically (KCl). They present the Frank–Starling mechanism, the Hill hyperbolic tension–velocity relationship, and the tridimensional time-independent tension–velocity–length relationship. Relaxation could be obtained by the inhibition of crossbridge molecular motors or by a decrease in the intracellular calcium concentration. They differ from muscles in that their kinetics are ultraslow as evidenced by their low shortening velocity and myosin ATPase activity. Contractility is generated by non-muscle myosin type II A and II B. The activation of the β-catenin/WNT pathway is accompanied by the high level of the non-muscle myosin observed in lung cancers. Full article
(This article belongs to the Special Issue Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms)
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18 pages, 19454 KiB  
Article
The Role of CCL24 in Primary Sclerosing Cholangitis: Bridging Patient Serum Proteomics to Preclinical Data
by Raanan Greenman, Tom Snir, Avi Katav, Revital Aricha, Inbal Mishalian, Ophir Hay, Matthew Frankel, John Lawler, Francesca Saffioti, Massimo Pinzani, Douglas Thorburn, Amnon Peled, Adi Mor and Ilan Vaknin
Cells 2024, 13(3), 209; https://doi.org/10.3390/cells13030209 - 23 Jan 2024
Viewed by 1538
Abstract
Primary sclerosing cholangitis (PSC) is an inflammatory and fibrotic biliary disease lacking approved treatment. We studied CCL24, a chemokine shown to be overexpressed in damaged bile ducts, and its involvement in key disease-related mechanisms. Serum proteomics of PSC patients and healthy controls (HC) [...] Read more.
Primary sclerosing cholangitis (PSC) is an inflammatory and fibrotic biliary disease lacking approved treatment. We studied CCL24, a chemokine shown to be overexpressed in damaged bile ducts, and its involvement in key disease-related mechanisms. Serum proteomics of PSC patients and healthy controls (HC) were analyzed using the Olink® proximity extension assay and compared based on disease presence, fibrosis severity, and CCL24 levels. Disease-related canonical pathways, upstream regulators, and toxicity functions were elevated in PSC patients compared to HC and further elevated in patients with high CCL24 levels. In vitro, a protein signature in CCL24-treated hepatic stellate cells (HSCs) differentiated patients by disease severity. In mice, CCL24 intraperitoneal injection selectively recruited neutrophils and monocytes. Treatment with CM-101, a CCL24-neutralizing antibody, in an α-naphthylisothiocyanate (ANIT)-induced cholestasis mouse model effectively inhibited accumulation of peribiliary neutrophils and macrophages while reducing biliary hyperplasia and fibrosis. Furthermore, in PSC patients, CCL24 levels were correlated with upregulation of monocyte and neutrophil chemotaxis pathways. Collectively, these findings highlight the distinct role of CCL24 in PSC, influencing disease-related mechanisms, affecting immune cells trafficking and HSC activation. Its blockade with CM-101 reduces inflammation and fibrosis and positions CCL24 as a promising therapeutic target in PSC. Full article
(This article belongs to the Special Issue Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms)
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13 pages, 2763 KiB  
Article
Daphnetin Alleviates Bleomycin-Induced Pulmonary Fibrosis through Inhibition of Epithelial-to-Mesenchymal Transition and IL-17A
by Soo-Jin Park, Hyung Won Ryu, Ji-Hyeong Kim, Hwa-Jeong Hahn, Hyun-Jae Jang, Sung-Kyun Ko, Sei-Ryang Oh and Hyun-Jun Lee
Cells 2023, 12(24), 2795; https://doi.org/10.3390/cells12242795 - 08 Dec 2023
Viewed by 1037
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there is no cure for IPF, the development of drugs with improved efficacy in the treatment of IPF is required. Daphnetin, a natural coumarin derivative, has immunosuppressive, anti-inflammatory, and antioxidant [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there is no cure for IPF, the development of drugs with improved efficacy in the treatment of IPF is required. Daphnetin, a natural coumarin derivative, has immunosuppressive, anti-inflammatory, and antioxidant activities. However, its antifibrotic effects have not yet been elucidated. In this study, we investigated the antifibrotic effects of daphnetin on pulmonary fibrosis and the associated molecular mechanism. We examined the effects of daphnetin on splenocytes cultured in Th17 conditions, lung epithelial cells, and a mouse model of bleomycin (BLM)-induced pulmonary fibrosis. We identified that daphnetin inhibited IL-17A production in developing Th17 cells. We also found that daphnetin suppressed epithelial-to-mesenchymal transition (EMT) in TGF-β-treated BEAS2B cells through the regulation of AKT phosphorylation. In BLM-treated mice, the oral administration of daphnetin attenuated lung histopathology and improved lung mechanical functions. Our findings clearly demonstrated that daphnetin inhibited IL-17A and EMT both in vitro and in vivo, thereby protecting against BLM-induced pulmonary fibrosis. Taken together, these results suggest that daphnetin has potent therapeutic effects on lung fibrosis by modulating both Th17 differentiation and the TGF-β signaling pathway, and we thus expect daphnetin to be a drug candidate for the treatment of IPF. Full article
(This article belongs to the Special Issue Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms)
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16 pages, 25170 KiB  
Article
Hypoxia-Induced HIF-1α Expression Promotes Neurogenic Bladder Fibrosis via EMT and Pyroptosis
by Qi Li, Yifan Hong, Jing Chen, Xiazhu Zhou, Xiaomao Tian, Yihang Yu, Lianju Shen, Chunlan Long, Miao Cai, Shengde Wu and Guanghui Wei
Cells 2022, 11(23), 3836; https://doi.org/10.3390/cells11233836 - 29 Nov 2022
Cited by 4 | Viewed by 2142
Abstract
Background: Neurogenic bladder (NB) patients exhibit varying degrees of bladder fibrosis, and the thickening and hardening of the bladder wall induced by fibrosis will further affect bladder function and cause renal failure. Our study aimed to investigate the mechanism of bladder fibrosis caused [...] Read more.
Background: Neurogenic bladder (NB) patients exhibit varying degrees of bladder fibrosis, and the thickening and hardening of the bladder wall induced by fibrosis will further affect bladder function and cause renal failure. Our study aimed to investigate the mechanism of bladder fibrosis caused by a spinal cord injury (SCI). Methods: NB rat models were created by cutting the bilateral lumbar 6 (L6) and sacral 1 (S1) spinal nerves. RNA-seq, Western blotting, immunofluorescence, cell viability and ELISA were performed to assess the inflammation and fibrosis levels. Results: The rats showed bladder dysfunction, upper urinary tract damage and bladder fibrosis after SCI. RNA-seq results indicated that hypoxia, EMT and pyroptosis might be involved in bladder fibrosis induced by SCI. Subsequent Western blot, ELISA and cell viability assays and immunofluorescence of bladder tissue confirmed the RNA-seq findings. Hypoxic exposure increased the expression of HIF-1α and induced EMT and pyroptosis in bladder epithelial cells. Furthermore, HIF-1α knockdown rescued hypoxia-induced pyroptosis, EMT and fibrosis. Conclusion: EMT and pyroptosis were involved in the development of SCI-induced bladder fibrosis via the HIF-1α pathway. Inhibition of the HIF-1α pathway may serve as a potential target to alleviate bladder fibrosis caused by SCI. Full article
(This article belongs to the Special Issue Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms)
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