Статті в журналах: "Fibrosis"

1

&NA;. "Cystic fibrosis and fibrosing colonopathy." Advances in Anatomic Pathology 3, no. 2 (March 1996): 112. http://dx.doi.org/10.1097/00125480-199603000-00015.

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2

Smyth, R. L. "Fibrosing colonopathy in cystic fibrosis." Archives of Disease in Childhood 74, no. 5 (May 1, 1996): 464–68. http://dx.doi.org/10.1136/adc.74.5.464.

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3

Hernandez-Gonzalez, Fernanda, Rosa Faner, Mauricio Rojas, Alvar Agustí, Manuel Serrano, and Jacobo Sellarés. "Cellular Senescence in Lung Fibrosis." International Journal of Molecular Sciences 22, no. 13 (June 29, 2021): 7012. http://dx.doi.org/10.3390/ijms22137012.

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Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.

4

Albera, Carlo, Giulia Verri, Federico Sciarrone, Elena Sitia, Mauro Mangiapia, and Paolo Solidoro. "Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective." Biomedicines 9, no. 9 (September 16, 2021): 1237. http://dx.doi.org/10.3390/biomedicines9091237.

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Interstitial lung diseases (ILDs) are a large and diverse group of rare and chronic respiratory disorders, with idiopathic pulmonary fibrosis (IPF) being the most common and best-studied member. Increasing interest in fibrosis as a therapeutic target and the appreciation that fibrotic mechanisms may be a treatable target of IPF prompted the development and subsequent approval of the antifibrotics, pirfenidone and nintedanib. The management of ILDs has changed considerably following an understanding that IPF and some ILDs share similar disease behavior of progressive fibrosis, termed “progressive fibrosing phenotype”. Indeed, antifibrotic treatment has shown to be beneficial in ILDs characterized by the progressive fibrosing phenotype. This narrative review summarizes current knowledge in the field of progressive fibrosing ILDs. Here, we discuss the clinical characteristics and pathogenesis of lung fibrosis and highlight relevant literature concerning the mechanisms underlying progressive fibrosing ILDs. We also summarize current diagnostic approaches and the available treatments of progressive fibrosing ILDs and address the optimization of treating progressive fibrosing ILDs with antifibrotics in clinical practice.

5

Waters, Brenda L. "Cystic Fibrosis with Fibrosing Colonopathy in the Absence of Pancreatic Enzymes." Pediatric and Developmental Pathology 1, no. 1 (January 1998): 74–78. http://dx.doi.org/10.1007/s100249900009.

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Fibrosing colonopathy, characterized by dense submucosal fibrosis in the large bowel, is a disorder associated with bowel dysfunction in patients with cystic fibrosis who receive pancreatic enzyme supplementation. Most commonly, patients present with a distended abdomen and abdominal pain. Radiographs frequently demonstrate colonic wall thickening and luminal narrowing. Here I describe a neonate with cystic fibrosis who presented with both clinical and histological features of fibrosing colonopathy who had not received pancreatic enzymes. This report expands our understanding of the pathogenesis of fibrosing colonopathy.

6

Gibson, Sarah E., Carol F. Farver, and Richard A. Prayson. "Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature." Archives of Pathology & Laboratory Medicine 130, no. 2 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.

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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.

7

Carrino, David A., Sam Mesiano, Nichole M. Barker, William W. Hurd, and Arnold I. Caplan. "Proteoglycans of uterine fibroids and keloid scars: similarity in their proteoglycan composition." Biochemical Journal 443, no. 2 (March 27, 2012): 361–68. http://dx.doi.org/10.1042/bj20111996.

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Fibrosis is the formation of excess and abnormal fibrous connective tissue as a result of either a reparative or reactive process. A defining feature of connective tissue is its extracellular matrix, which provides structural support and also influences cellular activity. Two common human conditions that result from fibrosis are uterine fibroids (leiomyomas) and keloid scars. Because these conditions share a number of similarities and because their growth is due primarily to excessive extracellular matrix deposition, we compared the proteoglycans of uterine fibroids and keloid scars with corresponding normal tissues. Our analysis indicates that uterine fibroids and keloid scars contain higher amounts of glycosaminoglycans relative to normal myometrium and normal adult skin respectively. Proteoglycan composition is also different in the fibrotic tissues. Compared with unaffected tissues, uterine fibroids and keloid scars contain higher relative amounts of versican and lower relative amounts of decorin. There is also evidence for a higher level of versican catabolism in the fibrotic tissues compared with unaffected tissues. These qualitative and quantitative proteoglycan differences may play a role in the expansion of these fibroses and in their excessive matrix deposition and matrix disorganization, due to effects on cell proliferation, TGF (transforming growth factor)-β signalling and/or collagen fibril formation.

8

Yu, Guoying. "Fibrosis: A New Open-Access Journal to Share Your Research." Fibrosis 1, no. 1 (2023): 1–2. http://dx.doi.org/10.35534/fibrosis.2023.10001.

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9

Cottin, Vincent, Lutz Wollin, Aryeh Fischer, Manuel Quaresma, Susanne Stowasser, and Sergio Harari. "Fibrosing interstitial lung diseases: knowns and unknowns." European Respiratory Review 28, no. 151 (February 27, 2019): 180100. http://dx.doi.org/10.1183/16000617.0100-2018.

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Patients with certain types of fibrosing interstitial lung disease (ILD) are at risk of developing a progressive phenotype characterised by self-sustaining fibrosis, decline in lung function, worsening quality of life, and early mortality. It has been proposed that such progressive fibrosing ILDs, which show commonalities in clinical behaviour and in the pathogenetic mechanisms that drive progressive fibrosis, may be “lumped” together for the purposes of clinical research and, potentially, for treatment. At present, no drugs are approved for the treatment of ILDs other than nintedanib and pirfenidone for the treatment of idiopathic pulmonary fibrosis. For other progressive fibrosing ILDs, the mainstay of drug therapy is immunosuppression. However, it is postulated that, once the response to lung injury in fibrosing ILDs has reached the stage at which fibrosis has become progressive and self-sustaining, targeted antifibrotic therapy would be required to slow disease progression. Nintedanib, an intracellular inhibitor of tyrosine kinases, has shown antifibrotic, anti-inflammatory and vascular remodelling effects in several non-clinical models of fibrosis, irrespective of the trigger for the injury. Ongoing clinical trials will provide insight into the role of antifibrotic treatment with nintedanib or pirfenidone in the management of fibrosing ILDs with a progressive phenotype.

10

Tsomidis, Ioannis, George Notas, Argyro Voumvouraki, Dimitrios Samonakis, Mairi Koulentaki, and Elias Kouroumalis. "Hepatic Lysosomal Enzyme Activity in Primary Biliary Cholangitis." Fibrosis 1, no. 1 (2023): 1–12. http://dx.doi.org/10.35534/fibrosis.2023.10005.

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11

Li, Zhongzheng, Huabin Zhao, Shenghui Wang, Peishuo Yan, Hongmei Yuan, Mengxia Zhao, Ruyan Wan, et al. "Comprehensive Landscape of Matrix Metalloproteinases in the Pathogenesis of Idiopathic Pulmonary Fibrosis." Fibrosis 1, no. 1 (2023): 1–14. http://dx.doi.org/10.35534/fibrosis.2023.10004.

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12

David, Elroei, Alina Karabchevsky, Marina Wolfson, and Vadim E. Fraifeld. "Pulsed Ultraviolet C as a Potential Treatment for COVID-19." Fibrosis 1, no. 1 (2023): 1–6. http://dx.doi.org/10.35534/fibrosis.2023.10002.

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13

Weiskirchen, Ralf. "Established Hepatic Stellate Cell Lines in Hepatology Research." Fibrosis 1, no. 1 (2023): 1–9. http://dx.doi.org/10.35534/fibrosis.2023.10003.

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14

Wang, Chao, Amlan Chakraborty, Deidree V. N. Somanader, Michael Nguyen, Chen Wei, Robert E. Widdop, and Chrishan S. Samuel. "The Severity of Isoproterenol-induced Myocardial Fibrosis and Related Dysfunction in Mice is Strain-dependent." Fibrosis 1, no. 2 (2023): 1–9. http://dx.doi.org/10.35534/fibrosis.2023.10006.

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15

Rius Rigau, Aleix, and Clara Dees. "Mechanisms of Fibroblast Activation during Fibrotic Tissue Remodeling." Fibrosis 2, no. 1 (2024): 10002. http://dx.doi.org/10.35534/fibrosis.2024.10002.

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16

Lamas, Santiago, Katalin Susztak, and Fernando Rodr韌uez-Pascual. "The Cellular and Metabolic Bases of Organ Fibrosis: UNIA Workshop 2023 in Baeza, Spain." Fibrosis 2, no. 1 (2024): 10001. http://dx.doi.org/10.35534/fibrosis.2024.10001.

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17

M. Artlett, Carol, and Lianne M. Connolly. "TANGO1 Dances to Export of Procollagen from the Endoplasmic Reticulum." Fibrosis 1, no. 2 (2023): 10008. http://dx.doi.org/10.35534/fibrosis.2023.10008.

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18

S. Espindola, Milena, David M. Habiel, Ana Lucia Coelho, Tanyalak Parimon, Peter Chen, Amanda Mikels-Vigdal, and Cory M. Hogaboam. "Translational Studies Reveal the Divergent Effects of Simtuzumab Targeting LOXL2 in Idiopathic Pulmonary Fibrosis." Fibrosis 1, no. 2 (2023): 1–12. http://dx.doi.org/10.35534/fibrosis.2023.10007.

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19

Pintér, István, Katalin Vágási, István Wittmann, and Judit Nagy. "Nephrogenic systemic fibrosis." Orvosi Hetilap 148, no. 38 (September 1, 2007): 1801–4. http://dx.doi.org/10.1556/oh.2007.28183.

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A nefrogén szisztémás fibrosis, melyet korábban nefrogén fibrotizáló dermopathiaként említett az irodalom, egy ritka kórkép, mely vesebetegeknél jelentkezik. A kialakulását elsősorban gadolínium alapú MRI-kontrasztanyag alkalmazását követően észlelték beszűkült vesefunkciójú, többnyire dializált betegeken. A nefrogén szisztémás fibrosist a végtagok distalis részén kezdődő, majd a súlyosabb esetekben a tüdőt, májat, szív- és vázizomzatot is érintő fibrosis jellemzi. A betegség több szervrendszer együttes érintettsége esetén – az esetek mintegy 5%-ában – gyors lefolyású és halálos kimenetelű is lehet. Bizonyítékokon alapuló terápiája még nem ismert, de egy-egy esetben javulást észleltek vesetranszplantáció és plazmaferézis után, illetve gyógyulást írtak le extracorporalis fotoferézist követően.

20

Khan, Khaleque N., Akira Fujishita, Akemi Koshiba, Kanae Ogawa, Taisuke Mori, Hiroshi Ogi, Kyoko Itoh, Satoshi Teramukai, and Jo Kitawaki. "Expression profiles of E/P receptors and fibrosis in GnRHa-treated and -untreated women with different uterine leiomyomas." PLOS ONE 15, no. 11 (November 13, 2020): e0242246. http://dx.doi.org/10.1371/journal.pone.0242246.

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Differential expressions of estrogen/progesterone receptors (ER/PR) and individual component of extracellular matrices derived from fibroid are reported. Information on the pattern of change in ER/PR expression and amount of tissue fibrosis after hormonal treatment is unclear. We investigated pattern of change in ER/PR expression and percentage of tissue fibrosis in different uterine leiomyomas after gonadotropin-releasing hormone agonist (GnRHa) treatment. Biopsy specimens from fibroids and adjacent myometria were collected after surgery from women with submucosal myoma (SMM, n = 18), intramural myoma (IMM, n = 16) and subserosal myoma (SSM, n = 17). A proportion of women in each group of fibroid underwent treatment with GnRHa for a variable period of 3–6 months. Tissue expression of ER and PR was analyzed by immunohistochemistry. In vitro cell proliferation effect of GnRHa on human umbilical vein endothelial cells (HUVECs) was examined. Distribution of tissue fibrosis was examined by Masson’s trichrome staining with computer-captured image analysis of fibrosis derived from different types of fibroid. PR content was significantly higher than ER in tissues derived from GnRHa-untreated women with SMM and SSM (p = 0.04 for both). Comparing to untreated group, GnRHa-treatment significantly decreased either ER or PR expression in different fibroids. Exogenous treatment with GnRHa dose-dependently decreased proliferation of HUVECs. No significant difference was observed in the percentage of fibrosis in tissues collected from GnRHa-treated and -untreated women with fibroids. The distribution of fibrosis in myoma/myometria and occurrence of fibrosis in perivascular area showed an increasing trend with higher age of the women and with larger size of fibroids. Our findings suggest that despite estrogen dependency, higher PR content in GnRHa-untreated group may indicate a potential role of progesterone in leiomyoma growth. Although GnRHa therapy may shrink fibroids and reduce risk of bleeding during surgery, the occurrence of diffuse tissue fibrosis may impair effective reduction of fibroid size after hormonal treatment.

21

D’Agnano, Vito, Domenica Francesca Mariniello, Michela Ruotolo, Gianluca Quarcio, Alessandro Moriello, Stefano Conte, Antonio Sorrentino, Stefano Sanduzzi Zamparelli, Andrea Bianco, and Fabio Perrotta. "Targeting Progression in Pulmonary Fibrosis: An Overview of Underlying Mechanisms, Molecular Biomarkers, and Therapeutic Intervention." Life 14, no. 2 (February 6, 2024): 229. http://dx.doi.org/10.3390/life14020229.

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Interstitial lung diseases comprise a heterogenous range of diffuse lung disorders, potentially resulting in pulmonary fibrosis. While idiopathic pulmonary fibrosis has been recognized as the paradigm of a progressive fibrosing interstitial lung disease, other conditions with a progressive fibrosing phenotype characterized by a significant deterioration of the lung function may lead to a burden of significant symptoms, a reduced quality of life, and increased mortality, despite treatment. There is now evidence indicating that some common underlying biological mechanisms can be shared among different chronic fibrosing disorders; therefore, different biomarkers for disease-activity monitoring and prognostic assessment are under evaluation. Thus, understanding the common pathways that induce the progression of pulmonary fibrosis, comprehending the diversity of these diseases, and identifying new molecular markers and potential therapeutic targets remain highly crucial assignments. The purpose of this review is to examine the main pathological mechanisms regulating the progression of fibrosis in interstitial lung diseases and to provide an overview of potential biomarker and therapeutic options for patients with progressive pulmonary fibrosis.

22

Bertero, Michele, Serena Bainotti, Alberto Comino, Marco Formica, Fabrizio Giordano, Luca Musso, Stefania Palazzini, and Zelda Seia. "Nephrogenic fibrosing dermopathy/nephrogenic systemic fibrosis." European Journal of Dermatology 19, no. 1 (January 2009): 073–74. http://dx.doi.org/10.1684/ejd.2008.0547.

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23

Prasad, Srinivasa R., and Jaishree Jagirdar. "Nephrogenic Systemic Fibrosis/Nephrogenic Fibrosing Dermopathy." Journal of Computer Assisted Tomography 32, no. 1 (January 2008): 1–3. http://dx.doi.org/10.1097/rct.0b013e31805d08ee.

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24

Galan, Anjela, Shawn E. Cowper, and Richard Bucala. "Nephrogenic systemic fibrosis (nephrogenic fibrosing dermopathy)." Current Opinion in Rheumatology 18, no. 6 (November 2006): 614–17. http://dx.doi.org/10.1097/01.bor.0000245725.94887.8d.

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25

Fellrath, J. M., and R. M. du Bois. "Idiopathic pulmonary fibrosis/cryptogenic fibrosing alveolitis." Clinical and Experimental Medicine 3, no. 2 (September 2003): 65–83. http://dx.doi.org/10.1007/s10238-003-0010-3.

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26

LYON, IAN C. T., and DIANNE R. WEBSTER. "Newborn Screening for Cystic Fibrosis." Pediatrics 87, no. 6 (June 1, 1991): 954–55. http://dx.doi.org/10.1542/peds.87.6.954.

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To the Editor.— The report on newborn screening for cystic fibrosis1 illustrates the need for continued evaluation of such programs. The authors state that the identification of cases of cystic fibrosis (CF) by an elevated level of immunoreactive trypsinogen (IRT) in second (follow-up) samples from infants with positive initial screening tests could result in false negatives in 27% of cases of cystic fibrosis without meconium ileus (MI). We have screened 401 122 infants using the method originally reported.2

27

Samokhodskaia, Larisa Mikhaylovna, Ekaterina Evgen'evna Starostina, Elena Borisovna Yarovaya, Tat'yana Nikolaevna Krasnova, Nikolay Alekseevich Mukhin, Vsevolod Arsen'evich Tkachuk, and Viktor Antonovich Sadovnichy. "Mathematic Model for Prediction of Liver Fibrosis Progression Rate in Patients with Chronic Hepatitis C Based on Combination of Genomic Markers." Annals of the Russian academy of medical sciences 70, no. 6 (December 3, 2015): 651–61. http://dx.doi.org/10.15690/vramn548.

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Aim of study. To evaluate clinical significance of different combinations of gene polymorphisms IL-1b, IL-6, IL-10, TNF, HFE, TGF-b, ATR1, NOS3894, CYBA, AGT, MTHFR, FII, FV, FVII, FXIII, ITGA2, ITGB3, FBG, PAI and their prognostic value for prediction of liver fibrosis progression rate in patients with chronic hepatitis C (CHC).Subjects and methods: 118 patients with CHC were divided into «fast» and «slow» (fibrosis rate progression ≥0,13 and 0,13 fibrosis units/yr; n =64 and n =54) fibrosis groups. Gene polymorphisms were determined. Statistical analysis was performed using Statistica 10.Results. A allele (p =0,012) and genotype AA (p =0,024) of AGT G-6T gene, as well as T allele (p =0,013) and MT+TT genotypes (p =0,005) of AGT 235 M/T gene were significantly more common in «fast fibrosers» than in «slow fibrosers». Patients with genotype TT of CYBA 242 C/T had a higher fibrosis progression rate than patients with CC+CT genotype (p =0,02). Our analysis showed a protective effect of TT genotype of ITGA2 807 C/T on fibrosis progression rate (p =0,03). There was a trend (p 0,15) to higher fibrosis progression rate in patients with mutant alleles and genotypes of TGFb +915 G/C, FXIII 103 G/T, PAI -675 5G/4G genes. Other gene polymorphisms were not associated with enhanced liver fibrosis. To build a mathematical model for prediction of liver fibrosis progression rate we performed coding with scores for genotypes and virus genotype. Total score correlated with the fibrosis progression rate (R =0,39, p =0,000).Conclusion: Determination of genetic profile of the patient and virus genotype allows to predict the course of CHC.

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Vijayakumar, Bavithra, and Pallav L. Shah. "Is Fibrosis Really Fibrosis?" American Journal of Respiratory and Critical Care Medicine 203, no. 11 (June 1, 2021): 1440–42. http://dx.doi.org/10.1164/rccm.202102-0334le.

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29

Ma, Hongge, Shupei Qiao, Zeli Wang, Shuai Geng, Yufang Zhao, Xiaolu Hou, Weiming Tian, Xiongbiao Chen, and Lifen Yao. "Microencapsulation of Lefty-secreting engineered cells for pulmonary fibrosis therapy in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 5 (May 1, 2017): L741—L747. http://dx.doi.org/10.1152/ajplung.00295.2016.

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Idiopathic pulmonary fibrosis (IPF) is a progressive disease that causes unremitting deposition of extracellular matrix proteins, thus resulting in distortion of the pulmonary architecture and impaired gas exchange. Associated with high morbidity and mortality, IPF is generally refractory to current pharmacological therapies. Lefty A, a potent inhibitor of transforming growth factor-β signaling, has been shown to have promising antifibrotic ability in vitro for the treatment of renal fibrosis and other potential organ fibroses. Here, we determined whether Lefty A can attenuate bleomycin (BLM)-induced pulmonary fibrosis in vivo based on a novel therapeutic strategy where human embryonic kidney 293 (HEK293) cells are genetically engineered with the Lefty A-associated GFP gene. The engineered HEK293 cells were encapsulated in alginate microcapsules and then subcutaneously implanted in ICR mice that had 1 wk earlier been intratracheally administered BLM to induce pulmonary fibrosis. The severity of fibrosis in lung tissue was assessed using pathological morphology and collagen expression to examine the effect of Lefty A released from the microencapsulated cells. The engineered HEK293 cells with Lefty A significantly reduced the expression of connective tissue growth factor and collagen type I mRNA, lessened the morphological fibrotic effects induced by BLM, and increased the expression of matrix metalloproteinase-9. This illustrates that engineered HEK293 cells with Lefty A can attenuate pulmonary fibrosis in vivo, thus providing a novel method to treat human pulmonary fibrotic disease and other organ fibroses.

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Huang, Chenyu, and Rei Ogawa. "The Vascular Involvement in Soft Tissue Fibrosis—Lessons Learned from Pathological Scarring." International Journal of Molecular Sciences 21, no. 7 (April 6, 2020): 2542. http://dx.doi.org/10.3390/ijms21072542.

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Soft tissue fibrosis in important organs such as the heart, liver, lung, and kidney is a serious pathological process that is characterized by excessive connective tissue deposition. It is the result of chronic but progressive accumulation of fibroblasts and their production of extracellular matrix components such as collagens. Research on pathological scars, namely, hypertrophic scars and keloids, may provide important clues about the mechanisms that drive soft tissue fibrosis, in particular the vascular involvement. This is because these dermal fibrotic lesions bear all of the fibrotic characteristics seen in soft tissue fibrosis. Moreover, their location on the skin surface means they are readily observable and directly treatable and therefore more accessible to research. We will focus here on the roles that blood vessel-associated cells play in cutaneous scar pathology and assess from the literature whether these cells also contribute to other soft tissue fibroses. These cells include endothelial cells, which not only exhibit aberrant functions but also differentiate into mesenchymal cells in pathological scars. They also include pericytes, hepatic stellate cells, fibrocytes, and myofibroblasts. This article will review with broad strokes the roles that these cells play in the pathophysiology of different soft tissue fibroses. We hope that this brief but wide-ranging overview of the vascular involvement in fibrosis pathophysiology will aid research into the mechanisms underlying fibrosis and that this will eventually lead to the development of interventions that can prevent, reduce, or even reverse fibrosis formation and/or progression.

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Solomon, Garron J., Elizabeth Wu, and Paul Peter Rosen. "Nephrogenic Systemic Fibrosis Mimicking Inflammatory Breast Carcinoma." Archives of Pathology & Laboratory Medicine 131, no. 1 (January 1, 2007): 145–48. http://dx.doi.org/10.5858/2007-131-145-nsfmib.

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Abstract Nephrogenic systemic fibrosis, previously known as nephrogenic fibrosing dermopathy, is a newly recognized systemic fibrosing disorder primarily affecting patients with chronic renal failure. Patients with skin involvement often develop papules and plaques with peau d'orange surface changes. The lower extremities and trunk are most commonly affected. The most important histologic differential diagnosis is with scleromyxedema. To our knowledge, we report the first case of nephrogenic systemic fibrosis involving the breasts of a 61-year-old woman with end-stage renal disease, clinically mimicking inflammatory breast carcinoma. We propose that nephrogenic systemic fibrosis be considered in the differential diagnosis as a rare possibility when cutaneous changes in the breast suggest inflammatory breast carcinoma in a patient with renal failure.

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Masuzaki, Ryota, Tatsuo Kanda, Reina Sasaki, Naoki Matsumoto, Masahiro Ogawa, Shunichi Matsuoka, Seth J. Karp, and Mitsuhiko Moriyama. "Noninvasive Assessment of Liver Fibrosis: Current and Future Clinical and Molecular Perspectives." International Journal of Molecular Sciences 21, no. 14 (July 11, 2020): 4906. http://dx.doi.org/10.3390/ijms21144906.

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Liver fibrosis is one of the risk factors for hepatocellular carcinoma (HCC) development. The staging of liver fibrosis can be evaluated only via a liver biopsy, which is an invasive procedure. Noninvasive methods for the diagnosis of liver fibrosis can be divided into morphological tests such as elastography and serum biochemical tests. Transient elastography is reported to have excellent performance in the diagnosis of liver fibrosis and has been accepted as a useful tool for the prediction of HCC development and other clinical outcomes. Two-dimensional shear wave elastography is a new technique and provides a real-time stiffness image. Serum fibrosis markers have been studied based on the mechanism of fibrogenesis and fibrolysis. In the healthy liver, homeostasis of the extracellular matrix is maintained directly by enzymes called matrix metalloproteinases (MMPs) and their specific inhibitors, tissue inhibitors of metalloproteinases (TIMPs). MMPs and TIMPs could be useful serum biomarkers for liver fibrosis and promising candidates for the treatment of liver fibrosis. Further studies are required to establish liver fibrosis-specific markers based on further clinical and molecular research. In this review, we summarize noninvasive fibrosis tests and molecular mechanism of liver fibrosis in current daily clinical practice.

33

Papiris, Spyros A., Panayiotis G. Vlachoyiannopoulos, Maria A. Maniati, Konstantinos X. Karakostas, Stavros H. Constantopoulos, and Haralampos H. Moutsopoulos. "Idiopathic Pulmonary Fibrosis and Pulmonary Fibrosis in Diffuse Systemic Sclerosis: Two Fibroses with Different Prognoses." Respiration 64, no. 1 (1997): 81–85. http://dx.doi.org/10.1159/000196648.

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34

Chaturvedi, Rachana, Tejal Shah, Amita Joshi, Toshi Mishra, Manjusha Karegar, and Akash Shukla. "Histopathological Study of Non-Cirrhotic Portal Fibrosis (NCPF) With Special Emphasis on Advanced Fibrosis." Annals of Pathology and Laboratory Medicine 2, no. 12 (December 17, 2018): A1002–1008. http://dx.doi.org/10.21276/apalm.2358.

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35

Patrucco, Filippo, Paolo Solidoro, Francesco Gavelli, Daria Apostolo, and Mattia Bellan. "Idiopathic Pulmonary Fibrosis and Post-COVID-19 Lung Fibrosis: Links and Risks." Microorganisms 11, no. 4 (March 30, 2023): 895. http://dx.doi.org/10.3390/microorganisms11040895.

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Idiopathic pulmonary fibrosis (IPF) is considered the paradigmatic example of chronic progressive fibrosing disease; IPF does not result from a primary immunopathogenic mechanism, but immune cells play a complex role in orchestrating the fibrosing response. These cells are activated by pathogen-associated or danger-associated molecular patterns generating pro-fibrotic pathways or downregulating anti-fibrotic agents. Post-COVID pulmonary fibrosis (PCPF) is an emerging clinical entity, following SARS-CoV-2 infection; it shares many clinical, pathological, and immune features with IPF. Similarities between IPF and PCPF can be found in intra- and extracellular physiopathological pro-fibrotic processes, genetic signatures, as well as in the response to antifibrotic treatments. Moreover, SARS-CoV-2 infection can be a cause of acute exacerbation of IPF (AE-IPF), which can negatively impact on IPF patients’ prognosis. In this narrative review, we explore the pathophysiological aspects of IPF, with particular attention given to the intracellular signaling involved in the generation of fibrosis in IPF and during the SARS-CoV-2 infection, and the similarities between IPF and PCPF. Finally, we focus on COVID-19 and IPF in clinical practice.

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D'Amico, A., V. Ficarra, A. Porcaro, R. Puce, S. Cicuto, G. Malossini, and C. Tallarigo. "L'eziopatogenesi della fibrosi retroperitoneale: Etiopathogenesis of retroperitoneal fibrosis." Urologia Journal 65, no. 2 (April 1998): 257–66. http://dx.doi.org/10.1177/039156039806500213.

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The etiopathogenesis of retroperitoneal fibrosis is still obscure and probably multifactorial. Among the secondary forms due to demonstrable causes, the one caused by aorto-iliac atherosclerosis has recently been recognised. Its pathogenesis is linked to the low density oxidised lipoproteins of the atheromatous plaque, which are responsible for a local immunologic reaction. The most common form is still idiopathic or primitive, hypothetically related to genetic, environmental, vascular and/or immunologic factors. Idiopathic retroperitoneal fibrosis is sometimes associated with other sclerosing syndromes and/or systemic diseases. In such cases a common pathogenesis, probably immunologic may be postulated. After having illustrated the different categories of retroperitoneal fibrosis, the authors report their experience with 25 patients of whom 14 had idiopathic fibrosis and 11 secondary fibrosis. In the former group 11 patients (78.5%) smoked more than 10 cigarettes a day, while there was a history of prolonged professional exposure to asbestos in one case. The following associated pathologies were observed: hypertension in 7 cases (50%), ischemic cardiopathy in 2 (14.3%), diabetes mellitus in 2 (14.3%), multiple myeloma in 1 (7.1%) and juvenile rheumatoid arthritis in 1 (7.1%). The disease was also associated with other sclerosing pathologies in 3 cases: sclerosing cholangitis in 2 and Dupuytren's contracture in 1. The location of the fibrosis was typically periaortic in 13 cases (92.8%), as shown by CT. Lastly, 10 patients underwent immunosuppressive therapy with a favourable response, suggesting the probable immunologic pathogenesis of the disease.

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Prakash, Sadhana, Amin A. Nanji, and Phillips W. Robbins. "Fibrosin: A Novel Lymphokine in Alcohol-Induced Fibrosis." Experimental and Molecular Pathology 67, no. 1 (September 1999): 40–49. http://dx.doi.org/10.1006/exmp.1999.2274.

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38

Brett, Allan S., and Elizabeth H. Mack. "Fibrosing Colonpathy in Adults with Cystic Fibrosis." American Journal of Roentgenology 190, no. 1 (January 2008): W73. http://dx.doi.org/10.2214/ajr.06.1589.

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39

Schwarzenberg, S. J., C. L. Wielinski, I. Shamieh, B. L. M. Carpenter, J. Jessurun, S. A. Weisdorf, W. J. Warwick, and H. L. Sharp. "Cystic fibrosis–associated colitis and fibrosing colonopathy." Journal of Pediatrics 127, no. 4 (October 1995): 565–70. http://dx.doi.org/10.1016/s0022-3476(95)70113-3.

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40

Littlewood, J. M. "Fibrosing colonopathy in children with cystic fibrosis." Postgraduate Medical Journal 72, no. 845 (March 1, 1996): 129–30. http://dx.doi.org/10.1136/pgmj.72.845.129.

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41

Reichard, Kirk W., Charles D. Vinocur, Maria Franco, Kristin L. Crisci, Jonathan A. Flick, Deborah F. Billmire, Daniel V. Schidlow, and William H. Weintraub. "Fibrosing colonopathy in children with cystic fibrosis." Journal of Pediatric Surgery 32, no. 2 (February 1997): 237–42. http://dx.doi.org/10.1016/s0022-3468(97)90186-x.

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42

Eddy, Allison A. "Scraping fibrosis: UMODulating renal fibrosis." Nature Medicine 17, no. 5 (May 2011): 553–55. http://dx.doi.org/10.1038/nm0511-553.

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43

Matai, V., S. Baer, S. Barnes, and M. Boxer. "Eosinophilic angiocentric fibrosis." Journal of Laryngology & Otology 114, no. 7 (July 2000): 563–64. http://dx.doi.org/10.1258/0022215001906183.

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Eosinophilic angiocentric fibrosis (EAF) is a rare inflammatory fibrosing condition of unknown aetiology that involves the nose or larynx producing mucosal thickening and severe obstructive symptoms. We report the first case affecting a male. He presented with nasal obstruction requiring septoplasty. The clinical and histopathological features of the condition are discussed and a comparison is made with the seven previous reported cases.

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Godil, Aamir, Kashif Gandhi, Mohammed Khan, and Arshi Kazi. "TOOTH PREPARATION IN ORAL SUB-MUCOUS FIBROSIS: CLINICAL TIPS." International Journal of Medical Reviews and Case Reports 4, Reports in Surgery, Urology and (2020): 1. http://dx.doi.org/10.5455/ijmrcr.submucous-fibrosis-tooth.

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45

Karhadkar, Tejas R., Wensheng Chen, Darrell Pilling, and Richard H. Gomer. "Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis." International Journal of Molecular Sciences 24, no. 1 (December 23, 2022): 239. http://dx.doi.org/10.3390/ijms24010239.

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Fibrosing diseases are a major medical problem, and are associated with more deaths per year than cancer in the US. Sialidases are enzymes that remove the sugar sialic acid from glycoconjugates. In this review, we describe efforts to inhibit fibrosis by inhibiting sialidases, and describe the following rationale for considering sialidases to be a potential target to inhibit fibrosis. First, sialidases are upregulated in fibrotic lesions in humans and in a mouse model of pulmonary fibrosis. Second, the extracellular sialidase NEU3 appears to be both necessary and sufficient for pulmonary fibrosis in mice. Third, there exist at least three mechanistic ways in which NEU3 potentiates fibrosis, with two of them being positive feedback loops where a profibrotic cytokine upregulates NEU3, and the upregulated NEU3 then upregulates the profibrotic cytokine. Fourth, a variety of NEU3 inhibitors block pulmonary fibrosis in a mouse model. Finally, the high sialidase levels in a fibrotic lesion cause an easily observed desialylation of serum proteins, and in a mouse model, sialidase inhibitors that stop fibrosis reverse the serum protein desialylation. This then indicates that serum protein sialylation is a potential surrogate biomarker for the effect of sialidase inhibitors, which would facilitate clinical trials to test the exciting possibility that sialidase inhibitors could be used as therapeutics for fibrosis.

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Zhang, Ranran, and William Nicholas Rose. "Photopheresis Provides Significant Long-Lasting Benefit in Nephrogenic Systemic Fibrosis." Case Reports in Dermatological Medicine 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/3240287.

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Nephrogenic systemic fibrosis (NSF), previously known as nephrogenic fibrosing dermopathy, is a rare complication of exposure to gadolinium-based contrast agents in patients who have significantly decreased renal function. Manifestations include fibrosis of the skin and other tissues. Effective therapies are lacking. Photopheresis has been tried with variable rates of improvement, and small numbers of cases (20 as of 2016) have been reported of NSF patients treated with photopheresis. We report a case of patient with nephrogenic systemic fibrosis who was treated with photopheresis and demonstrated significant lasting improvements.

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Slany Natarajan Kannan, Maggi. "Evaluation of Salivary Lactate Dehydrogenase in Oral Submucous Fibrosis & Its Correlation with Clinical Submucous Fibrosis." International Journal of Science and Research (IJSR) 12, no. 4 (April 5, 2023): 1242–44. http://dx.doi.org/10.21275/sr23419161537.

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48

Gavrysyuk, V. K., Y. O. Dziublyk, E. O. Merenkova, O. V. Strafun, and O. V. Bychenko. "PROGRESSIVE PULMONARY FIBROSIS IN LIGHT OF THE ATS/ERS/JRS/ALAT 2022 CLINICAL GUIDELINES." Ukrainian Pulmonology Journal 30, no. 4 (2022): 51–57. http://dx.doi.org/10.31215/2306-4927-2022-30-4-51-57.

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Idiopathic pulmonary fibrosis – is a specific form of chronic, progressive, fibrosing interstitial pneumonia of unknown cause, which occurs primarily in 50 years and older patients, limited to the lungs, and is associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP). In 2000 American thoracic society (ATS) and European respiratory society (ERS) published the first international; statement on diagnosis and treatment of IPF American Thoracic Society, European Respiratory Society. Idiopathic pulmonary fibrosis: diagnosis and treatment. International consensus statement. In 2011 there was published a new statement on diagnosis and treatment of IPF, approved by Japan respiratory society (JTS) and Latin American thoracis society (ALTS) – An Official ATS/ERS/JRS/AL : Idiopathic Pulmonary Fibrosis: Evidence-based Guidelines for Diagnosis and Management. In 2015 section “Treatment” and in 2018 section “Diagnosis” were revised. It is known that in part of patients with such interstitial lung diseases (ILD) as idiopathic interstitial pneumonia, systemic sclerosis, pneumoconiosis, chronic hypersensitivity pneumonitis, sarcoidosis the disease may acquire a progressive uncontrolled development with the combination of symptoms called progressive pulmonary fibrosis (PPF). At the same time the results of successful use of antifibrotic therapy have been published recently (SENSCIS, INBUILD studies). All this provided the rationale for extended indications for use of antifibrotic therapy to cover other ILDs with the features of PPF. In this connection, ATS, ERS, JRS and ALAT experts published in May 2022 An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline. Idiopathic Pulmonary Fibrosis (an Update) and Progressive Pulmonary Fibrosis in Adults, in which along with the partial changes regarding the principles of diagnosis and treatment of IPF, the definition, diagnosis criteria and management of PPF due to other fibrosing ILDs were presented. The article presents the major statements of new guideline regarding the terminology, diagnosis and treatment of PPF. Key words: progressive pulmonary fibrosis, definition, diagnosis criteria, treatment.

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Holtze, Colin, Kevin Flaherty, Michael Kreuter, Fabrizio Luppi, Teng Moua, Carlo Vancheri, and Mary B. Scholand. "Healthcare utilisation and costs in the diagnosis and treatment of progressive-fibrosing interstitial lung diseases." European Respiratory Review 27, no. 150 (December 21, 2018): 180078. http://dx.doi.org/10.1183/16000617.0078-2018.

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There are over 200 interstitial lung diseases (ILDs). In addition to patients with idiopathic pulmonary fibrosis (IPF), a percentage of patients with other ILDs also develop progressive fibrosis of the lung during their disease course. Patients with progressive-fibrosing ILDs may show limited response to immunomodulatory therapy, worsening symptoms and lung function and, ultimately, early mortality. There are few data for ILDs that may present a progressive fibrosing phenotype specifically, but we believe the burden and healthcare costs associated with these conditions may be comparable to those reported in IPF. This review discusses the burden of ILDs that may present a progressive fibrosing phenotype and the factors impacting healthcare utilisation.

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Takemura, Shigekazu, Hideki Azuma, Mayuko Osada-Oka, Shoji Kubo, Toshihiko Shibata, and Yukiko Minamiyama. "S-allyl-glutathione improves experimental liver fibrosis by regulating Kupffer cell activation in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 2 (February 1, 2018): G150—G163. http://dx.doi.org/10.1152/ajpgi.00023.2017.

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S-allyl-glutathione (SAG) is one of the metabolites of diallyl sulfide (DAS), a component of garlic. DAS has shown preventative effects on carcinogenesis in animal models. However, whether synthetic SAG can improve liver fibrosis has not been investigated. We examined the potential preventive effects of SAG on acute and chronic models of liver fibrosis by chronic carbon tetrachloride (CCl4) administration. SAG inhibited liver fibrogenesis induced by CCl4 in a dose-dependent manner and reduced heat shock protein-47 (HSP47), a collagen-specific chaperone, and other fibrosis markers. In fibrosis regression models, after administration of either CCl4 for 9 wk or dimethyl nitrosamine (DMN) for 6 wk, SAG markedly accelerated fibrolysis in both models. In the regression stage of DMN-treated liver, SAG normalized the ratio of M2 phenotype (expression of mannose receptor) in Kupffer cells (KCs). Consistent with these results, the culture supernatants of SAG-treated M2-phenotype KCs inhibited collagen-α1(I) chain (COL1A1) mRNA expression in primary culture-activated rat hepatic stellate cells (HSCs). However, SAG did not directly inhibit HSC activation. In an acute model of CCl4 single injection, SAG inhibited hepatic injury dose dependently consistent with the inhibited the elevation of the bilirubin and ALT levels. These findings suggest that SAG could improve the fibrogenic and fibrolysis cascade via the regulation of excess activated and polarized KCs. SAG may also serve as a preventive and therapeutic agent in fibrosis of other organs for which current clinical therapy is unavailable. NEW & NOTEWORTHY S-allyl-glutathione (SAG) is a metabolite of diallyl sulfide, a component of garlic. SAG increased hepatic glutathione levels and GSH-to-GSSG ratio in normal rats. SAG treatment before or after liver fibrosis from chronic CCl4 administration improved liver fibrosis and regression. SAG decreased heat shock protein-47 (HSP47), a collagen-specific chaperone, and other fibrosis markers in CCl4-treated livers. SAG-treated Kupffer cell conditioned medium also inhibited collagen-α1(I) chain (COL1A1) mRNA expression and other markers in primary culture hepatic stellate cells.

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