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Recent Advances in Pathophysiology of Fibrosis and Scarring 2020

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: closed (31 October 2020) | Viewed by 17696

Special Issue Editor


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Guest Editor
Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo 113-8603, Japan
Interests: burn reconstruction; scar management; keloid; hypertrophic scars; scar contractures
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Special Issue Information

I am honored to present the Special Issue of the International Journal of Molecular Sciences called “Recent Advances in Pathophysiology of Fibrosis and Scarring”, which will be published in 2020 and for which we are seeking contributors.

Fibrosis is the generation of fibrous connective tissues. It can be pathological when it interferes with organ architecture and functions. It arises from inflammation that is caused by a variety of mechanisms, including autoimmune reactions. It can also be initiated by wounding or damage, in which case it leads to scarring. Fibrosis and scarring involve complex biological pathways. Despite considerable research, the exact mechanisms by which these responses are initiated, evolve, and are regulated remain to be fully elucidated. Further research on these issues is important, because the development of effective treatments or strategies that prevent or halt fibrosis and induce scar-less wound healing would be a dramatic step forward for medical science. To achieve this goal, it is necessary to elucidate the relevant clinical, histopathological, and molecular manifestations of fibrosis and scarring and to understand how these manifestations relate to each other.

This Special Issue will cover a selection of recent research topics and will include current review articles in the field of fibrosis and scar research for all kinds of tissues and organs. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Prof. Dr. Rei Ogawa
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

  • Scar
  • Fibrosis
  • Fibroproliferative disorder
  • Inflammation
  • Organ fibrosis
  • Interstitial fibrosis
  • Arteriosclerosis
  • Keloids
  • Hypertrophic scars
  • Scleroderma
  • Pulmonary fibrosis
  • Cirrhosis
  • Nephrosclerosis

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Published Papers (3 papers)

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Research

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18 pages, 6927 KiB  
Article
Adipose-Derived Stem Cells Promote Intussusceptive Lymphangiogenesis by Restricting Dermal Fibrosis in Irradiated Tissue of Mice
by Ryohei Ogino, Kenji Hayashida, Sho Yamakawa and Eishin Morita
Int. J. Mol. Sci. 2020, 21(11), 3885; https://doi.org/10.3390/ijms21113885 - 29 May 2020
Cited by 25 | Viewed by 3604
Abstract
Currently, there is no definitive treatment for lymphatic disorders. Adipose-derived stem cells (ADSCs) have been reported to promote lymphatic regeneration in lymphedema models, but the mechanisms underlying the therapeutic effects remain unclear. Here, we tested the therapeutic effects of ADSC transplantation on lymphedema [...] Read more.
Currently, there is no definitive treatment for lymphatic disorders. Adipose-derived stem cells (ADSCs) have been reported to promote lymphatic regeneration in lymphedema models, but the mechanisms underlying the therapeutic effects remain unclear. Here, we tested the therapeutic effects of ADSC transplantation on lymphedema using a secondary lymphedema mouse model. The model was established in C57BL/6J mice by x-irradiation and surgical removal of the lymphatic system in situ. The number of lymphatic vessels with anti-lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) immunoreactivity increased significantly in mice subjected to transplantation of 7.5 × 105 ADSCs. X-irradiation suppressed lymphatic vessel dilation, which ADSC transplantation could mitigate. Proliferative cell nuclear antigen staining showed increased lymphatic endothelial cell (LEC) and extracellular matrix proliferation. Picrosirius red staining revealed normal collagen fiber orientation in the dermal tissue after ADSC transplantation. These therapeutic effects were not related to vascular endothelial growth factor (VEGF)-C expression. Scanning electron microscopy revealed structures similar to the intraluminal pillar during intussusceptive angiogenesis on the inside of dilated lymphatic vessels. We predicted that intussusceptive lymphangiogenesis occurred in lymphedema. Our findings indicate that ADSC transplantation contributes to lymphedema reduction by promoting LEC proliferation, improving fibrosis and dilation capacity of lymphatic vessels, and increasing the number of lymphatic vessels via intussusceptive lymphangiogenesis. Full article
(This article belongs to the Special Issue Recent Advances in Pathophysiology of Fibrosis and Scarring 2020)
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Review

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23 pages, 7254 KiB  
Review
Congestive Hepatopathy
by José Ignacio Fortea, Ángela Puente, Antonio Cuadrado, Patricia Huelin, Raúl Pellón, Francisco José González Sánchez, Marta Mayorga, María Luisa Cagigal, Inés García Carrera, Marina Cobreros, Javier Crespo and Emilio Fábrega
Int. J. Mol. Sci. 2020, 21(24), 9420; https://doi.org/10.3390/ijms21249420 - 10 Dec 2020
Cited by 34 | Viewed by 8602
Abstract
Liver disease resulting from heart failure (HF) has generally been referred as “cardiac hepatopathy”. One of its main forms is congestive hepatopathy (CH), which results from passive venous congestion in the setting of chronic right-sided HF. The current spectrum of CH differs from [...] Read more.
Liver disease resulting from heart failure (HF) has generally been referred as “cardiac hepatopathy”. One of its main forms is congestive hepatopathy (CH), which results from passive venous congestion in the setting of chronic right-sided HF. The current spectrum of CH differs from earlier reports with HF, due to ischemic cardiomyopathy and congenital heart disease having surpassed rheumatic valvular disease. The chronic passive congestion leads to sinusoidal hypertension, centrilobular fibrosis, and ultimately, cirrhosis (“cardiac cirrhosis”) and hepatocellular carcinoma after several decades of ongoing injury. Contrary to primary liver diseases, in CH, inflammation seems to play no role in the progression of liver fibrosis, bridging fibrosis occurs between central veins to produce a “reversed lobulation” pattern and the performance of non-invasive diagnostic tests of liver fibrosis is poor. Although the clinical picture and prognosis is usually dominated by the underlying heart condition, the improved long-term survival of cardiac patients due to advances in medical and surgical treatments are responsible for the increased number of liver complications in this setting. Eventually, liver disease could become as clinically relevant as cardiac disease and further complicate its management. Full article
(This article belongs to the Special Issue Recent Advances in Pathophysiology of Fibrosis and Scarring 2020)
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14 pages, 1860 KiB  
Review
A Tale of Two Proteolytic Machines: Matrix Metalloproteinases and the Ubiquitin–Proteasome System in Pulmonary Fibrosis
by Willy Roque, Alexandra Boni, Jose Martinez-Manzano and Freddy Romero
Int. J. Mol. Sci. 2020, 21(11), 3878; https://doi.org/10.3390/ijms21113878 - 29 May 2020
Cited by 11 | Viewed by 4996
Abstract
Pulmonary fibrosis is a chronic and progressive lung disease characterized by the activation of fibroblasts and the irreversible deposition of connective tissue matrices that leads to altered pulmonary architecture and physiology. Multiple factors have been implicated in the pathogenesis of lung fibrosis, including [...] Read more.
Pulmonary fibrosis is a chronic and progressive lung disease characterized by the activation of fibroblasts and the irreversible deposition of connective tissue matrices that leads to altered pulmonary architecture and physiology. Multiple factors have been implicated in the pathogenesis of lung fibrosis, including genetic and environmental factors that cause abnormal activation of alveolar epithelial cells, leading to the development of complex profibrotic cascade activation and extracellular matrix (ECM) deposition. One class of proteinases that is thought to be important in the regulation of the ECM are the matrix metalloproteinases (MMPs). MMPs can be up- and down- regulated in idiopathic pulmonary fibrosis (IPF) lungs and their role depends upon their location and function. Furthermore, alterations in the ubiquitin-proteosome system (UPS), a major intracellular protein degradation complex, have been described in aging and IPF lungs. UPS alterations could potentially lead to the abnormal accumulation and deposition of ECM. A better understanding of the specific roles MMPs and UPS play in the pathophysiology of pulmonary fibrosis could potentially drive to the development of novel biomarkers that can be as diagnostic and therapeutic targets. In this review, we describe how MMPs and UPS alter ECM composition in IPF lungs and mouse models of pulmonary fibrosis, thereby influencing the alveolar epithelial and mesenchymal cell behavior. Finally, we discuss recent findings that associate MMPs and UPS interplay with the development of pulmonary fibrosis. Full article
(This article belongs to the Special Issue Recent Advances in Pathophysiology of Fibrosis and Scarring 2020)
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