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Artículos de revistas sobre el tema "Fibrosis"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 25 de julio de 2025

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1

&NA;. "Cystic fibrosis and fibrosing colonopathy." Advances in Anatomic Pathology 3, no. 2 (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 (1996): 464–68. http://dx.doi.org/10.1136/adc.74.5.464.

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3

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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4

Moreno Diaz, Claudia, Estrella Caballeria, and Jacobo Sellar閟 Torres. "Comparative Analysis of Idiopathic Pulmonary Fibrosis and Progressive Pulmonary Fibrosis: Epidemiology, Pathophysiology, Clinical Features, Diagnosis and Treatment." Fibrosis 3, no. 1 (2025): 10001. https://doi.org/10.70322/fibrosis.2025.10001.

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5

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 (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 corre
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6

Khan, Khaleque N., Akira Fujishita, Akemi Koshiba, et al. "Expression profiles of E/P receptors and fibrosis in GnRHa-treated and -untreated women with different uterine leiomyomas." PLOS ONE 15, no. 11 (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), intramu
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7

Sferrazza, Sandro, Marcello Maida, Giulio Calabrese, et al. "The Derivation and External Validation of a Fibrosis Risk Model for Colorectal Tumours Undergoing Endoscopic Submucosal Dissection." Journal of Clinical Medicine 13, no. 15 (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
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8

Pintér, István, Katalin Vágási, István Wittmann, and Judit Nagy. "Nephrogenic systemic fibrosis." Orvosi Hetilap 148, no. 38 (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
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9

Samokhodskaia, Larisa Mikhaylovna, Ekaterina Evgen'evna Starostina, Elena Borisovna Yarovaya, et al. "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 (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.Res
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10

Bertero, Michele, Serena Bainotti, Alberto Comino, et al. "Nephrogenic fibrosing dermopathy/nephrogenic systemic fibrosis." European Journal of Dermatology 19, no. 1 (2009): 073–74. http://dx.doi.org/10.1684/ejd.2008.0547.

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11

du Bois, R. M., and A. U. Wells. "Cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis." European Respiratory Journal 18, no. 32 suppl (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
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12

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

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13

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

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14

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

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15

Ma, Hongge, Shupei Qiao, Zeli Wang, et al. "Microencapsulation of Lefty-secreting engineered cells for pulmonary fibrosis therapy in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 5 (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)-
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16

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 (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 chara
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17

Masuzaki, Ryota, Tatsuo Kanda, Reina Sasaki, et al. "Noninvasive Assessment of Liver Fibrosis: Current and Future Clinical and Molecular Perspectives." International Journal of Molecular Sciences 21, no. 14 (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 techn
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18

LYON, IAN C. T., and DIANNE R. WEBSTER. "Newborn Screening for Cystic Fibrosis." Pediatrics 87, no. 6 (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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19

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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20

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

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21

D'Amico, A., V. Ficarra, A. Porcaro, et al. "L'eziopatogenesi della fibrosi retroperitoneale: Etiopathogenesis of retroperitoneal fibrosis." Urologia Journal 65, no. 2 (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
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22

Li, Zhenwei, Zhao Zhu, Jiawei Wang, et al. "Exploring the Potential Relationship between Gut Microbiome Metabolites and Idiopathic Pulmonary Fibrosis via Network Pharmacology Study." Fibrosis 2, no. 4 (2024): 10009. http://dx.doi.org/10.70322/fibrosis.2024.10009.

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23

Wang, Yanrong, Zuhao Li, Chenyang Zhang, Ziqi Jin, and Adam C. Midgley. "Dermal Fibrosis and the Current Scope of Hydrogel Strategies for Scarless Wound Healing." Fibrosis 2, no. 4 (2024): 10010. http://dx.doi.org/10.70322/fibrosis.2024.10010.

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24

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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25

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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26

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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27

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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28

Guo, Xiaoshu, Yue Zhang, Yingjie Wang, et al. "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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29

Victorovich Garbuzenko, Dmitry. "Perspectives of Drug Therapy for Non-Alcoholic Steatohepatitis-Related Liver Fibrosis." Fibrosis 3, no. 1 (2025): 10002. https://doi.org/10.70322/fibrosis.2025.10002.

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30

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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31

Li, Zhongzheng, Huabin Zhao, Shenghui Wang, 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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32

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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33

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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34

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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35

S. Espindola, Milena, David M. Habiel, Ana Lucia Coelho, et al. "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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36

Wang, Chao, Amlan Chakraborty, Deidree V. N. Somanader, et al. "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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37

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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38

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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39

Weiskirchen, Ralf, and Amedeo Lonardo. "Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis (MASH)." Fibrosis 3, no. 2 (2025): 10005. https://doi.org/10.70322/fibrosis.2025.10005.

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40

M. Sofroniou, Michael, та Christopher A. Lemmon. "Mechanics and Synergistic Signaling of Fibronectin, Integrins, and TGF-β Isoforms". Fibrosis 3, № 1 (2025): 10003–4. https://doi.org/10.70322/fibrosis.2025.10003.

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41

Liu, Hongli, Huachun Cui, and Gang Liu. "The Intersection between Immune System and Idiopathic Pulmonary Fibrosis—A Concise Review." Fibrosis 3, no. 1 (2025): 10004. https://doi.org/10.70322/fibrosis.2025.10004.

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42

M. McFalls, Caya, and Carol M. Artlett. "NLRP3 Inflammasome and IL-11 in Systemic Sclerosis Pulmonary Fibroblasts." Fibrosis 3, no. 2 (2025): 10006. https://doi.org/10.70322/fibrosis.2025.10006.

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43

Castellani, Carson, Gregory Capelli, and Bryan S. Benn. "Time Is Lung: Inpatient Transbronchial Lung Cryobiopsy Decreases Wait Time to Treatment Initiation for Newly Diagnosed Interstitial Lung Disease." Fibrosis 3, no. 2 (2025): 10007. https://doi.org/10.70322/fibrosis.2025.10007.

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44

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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45

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 (2018): A1002–1008. http://dx.doi.org/10.21276/apalm.2358.

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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 (1999): 40–49. http://dx.doi.org/10.1006/exmp.1999.2274.

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47

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

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48

Schwarzenberg, S. J., C. L. Wielinski, I. Shamieh, et al. "Cystic fibrosis–associated colitis and fibrosing colonopathy." Journal of Pediatrics 127, no. 4 (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 (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, et al. "Fibrosing colonopathy in children with cystic fibrosis." Journal of Pediatric Surgery 32, no. 2 (1997): 237–42. http://dx.doi.org/10.1016/s0022-3468(97)90186-x.

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