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Статті в журналах з теми "Fibrosis"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 16 листопада 2024

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1

Egea-Zorrilla, Alejandro, Zuri馿 Blasco-Iturri, Borja Saez, and Ana Pardo-Saganta. "The Notch3 Pathway in Organ Fibrosis." Fibrosis 2, no. 4 (2024): 10007. http://dx.doi.org/10.70322/fibrosis.2024.10007.

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2

&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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3

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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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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Анотація:

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.

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5

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.

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6

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.

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7

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.

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8

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.

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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.

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10

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.

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11

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.

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12

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.

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13

Sferrazza, Sandro, Marcello Maida, Giulio Calabrese, Antonio Facciorusso, Lorenzo Fuccio, Leonardo Frazzoni, Roberta Maselli, Alessandro Repici, Roberto Di Mitri, and João Santos-Antunes. "The Derivation and External Validation of a Fibrosis Risk Model for Colorectal Tumours Undergoing Endoscopic Submucosal Dissection." Journal of Clinical Medicine 13, no. 15 (August 2, 2024): 4517. http://dx.doi.org/10.3390/jcm13154517.

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Background: Endoscopic submucosal dissection (ESD) is an advanced technique that can become more challenging in the presence of submucosal fibrosis. Predicting the grade of fibrosis is important in order to identify technically difficult ESD. Aims and Methods: Our study aimed to derive and validate a prediction model to determine the preoperative degree of submucosal fibrosis in colorectal tumours undergoing ESD. A predictive model was developed to derive the probability of an increasing submucosal fibrosis in the derivation cohort and then externally validated. Results: 309 patients (age: 68 ± 10.9 years) underwent colorectal ESD between January 2016 and June 2020. F0, F1, and F2 fibroses were reported in 196 (63.4%), 70 (22.6%), and 43 (13.9%) cases, respectively. R0 resection was found in 266 (87%) lesions. At multivariable analysis in the derivation cohort, lesion morphology (OR = 0.37 and CI = 0.14–0.97 for LST-NG vs. 0-Is; OR = 0.29 and CI = 0.1–0.87 for the LST mixed type vs. 0-Is; and OR = 0.32 and CI = 0.1–1.03 for LST-G vs. 0-Is) and increasing size (OR = 1.02 and CI = 1.01–1.04 for a 1 mm increase) were significantly associated with an increasing degree of fibrosis. The model had fair discriminating ability in the derivation group (AUROC = 0.61 and CI = 0.52–0.69 for F1–F2 vs. F0 fibroses; AUROC = 0.61 and CI = 0.45–0.77 for F2 vs. F0–F1 fibroses) and in the validation group (AUROC = 0.71 and CI = 0.59–0.83 for F1–F2 vs. F0 fibroses; AUROC = 0.65 and CI = 0.52–0.77 for F2 vs. F0–F1 fibroses). Conclusions: Our findings introduce a new tool for the stratification of ESD technical difficulty based on lesion size and morphological characteristics which could become crucial during the procedure’s planning process.

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14

Hernandez-Gonzalez, Fernanda, Federico Pietrocola, Paolo Cameli, Elena Bargagli, Sergio Prieto-González, Tamara Cruz, Nuria Mendoza, et al. "Exploring the Interplay between Cellular Senescence, Immunity, and Fibrosing Interstitial Lung Diseases: Challenges and Opportunities." International Journal of Molecular Sciences 25, no. 14 (July 10, 2024): 7554. http://dx.doi.org/10.3390/ijms25147554.

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Fibrosing interstitial lung diseases (ILDs) are characterized by the gradual and irreversible accumulation of scar tissue in the lung parenchyma. The role of the immune response in the pathogenesis of pulmonary fibrosis remains unclear. In recent years, substantial advancements have been made in our comprehension of the pathobiology driving fibrosing ILDs, particularly concerning various age-related cellular disturbances and immune mechanisms believed to contribute to an inadequate response to stress and increased susceptibility to lung fibrosis. Emerging studies emphasize cellular senescence as a key mechanism implicated in the pathobiology of age-related diseases, including pulmonary fibrosis. Cellular senescence, marked by antagonistic pleiotropy, and the complex interplay with immunity, are pivotal in comprehending many aspects of lung fibrosis. Here, we review progress in novel concepts in cellular senescence, its association with the dysregulation of the immune response, and the evidence underlining its detrimental role in fibrosing ILDs.

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15

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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16

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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17

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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18

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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19

du Bois, R. M., and A. U. Wells. "Cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis." European Respiratory Journal 18, no. 32 suppl (January 1, 2001): 43S—55S. http://dx.doi.org/10.1183/09031936.01.18s320043.

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Cryptogenic fibrosing alveolitis (CFA), synonymous with idiopathic pulmonary fibrosis (IPF), remains a life-threatening disease: 50% of patients die within 5 yrs. Historically, many diseases that are now considered to be quite distinct have been “labelled” as CFA. More recently, high-resolution computed tomography and new appreciation of the histopathological patterns of idiopathic interstitial pneumonias have enabled disease variants to be defined according to their different responses to therapy and survival.CFA is believed to be induced by an external agent, although it is not clear whether CFA represents the final common outcome of numerous pathogenetic mechanisms or has a single cause. In addition, there are currently no prospective double-blind, placebo-controlled trials of treatment showing superiority of one drug regimen over another.This review attempts to dissect the different patterns of cryptogenic fibrosing alveolitis, illustrate the major features of each, and refine the clinico-radiological-pathological descriptors that together define cryptogenic fibrosing alveolitis as it is understood today.

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20

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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21

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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22

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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23

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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24

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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25

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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26

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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27

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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28

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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29

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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30

Weiskirchen, Ralf, H鍁ard Attramadal, and Bernard Perbal. "12th International Workshop on the CCN Family of Genes." Fibrosis 2, no. 1 (2024): 10003. http://dx.doi.org/10.35534/fibrosis.2024.10003.

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31

Guo, Xiaoshu, Yue Zhang, Yingjie Wang, Xin Pan, Cong Xia, Zhongzheng Li, Huibing Liu, Ralf Weiskirchen, and Guoying Yu. "Mitochondrial Damage and Epithelial-Mesenchymal Transition as Major Triggers of the Development of Idiopathic Pulmonary Fibrosis." Fibrosis 2, no. 1 (2024): 10004. http://dx.doi.org/10.35534/fibrosis.2024.10004.

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32

R. Lapthorn, Alice, Sophie L. Harding, Kieran M. Feltham, Deepika Sathyananth, Daniel C. Salisbury, and Selim Cellek. "A Review of the Current Landscape of Anti-Fibrotic Medicines." Fibrosis 2, no. 1 (2024): 10005. http://dx.doi.org/10.70322/fibrosis.2024.10005.

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33

Jamalinia, Mohamad, Amedeo Lonardo, and Ralf Weiskirchen. "Sex and Gender Differences in Liver Fibrosis: Pathomechanisms and Clinical Outcomes." Fibrosis 2, no. 1 (2024): 10006. http://dx.doi.org/10.70322/fibrosis.2024.10006.

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34

Arevalo, Carlo, and David J. Nagel. "Acute Exacerbations of Interstitial Lung Disease: Evolving Perspectives on Diagnosis and Management." Fibrosis 2, no. 4 (2024): 10008. http://dx.doi.org/10.70322/fibrosis.2024.10008.

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35

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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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

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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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38

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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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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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.

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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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43

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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44

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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46

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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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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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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49

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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50

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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