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Academic literature on the topic 'Antifibrotics'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Antifibrotics"

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Niitsu, Takayuki, Kiyoharu Fukushima, Sho Komukai, So Takata, Yuko Abe, Takuro Nii, Tomoki Kuge, et al. "Real-world impact of antifibrotics on prognosis in patients with progressive fibrosing interstitial lung disease." RMD Open 9, no. 1 (January 2023): e002667. http://dx.doi.org/10.1136/rmdopen-2022-002667.

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ObjectiveNo studies have demonstrated the real-world efficacy of antifibrotics for progressive fibrosing interstitial lung disease (PF-ILD). Therefore, we evaluated the efficacy of antifibrotics in patients with PF-ILD.MethodsWe retrospectively reviewed the medical records of patients with ILD from January 2012 to July 2021. Patients were diagnosed with PF-ILD if they had ≥10% fibrosis on high-resolution CT (HRCT) and a relative forced vital capacity (FVC) decline of either ≥10% or >5% to <10% with clinical deterioration or progression of fibrosis on HRCT during overlapping windows of 2 years and with a %FVC of ≥45%. We compared FVC changes and overall survival (OS) between patients with and without antifibrotics. FVC changes were analysed using generalised estimating equations. We used inverse probability weighting (IPW) and statistical matching to adjust for covariates.ResultsOf the 574 patients, 167 were diagnosed with PF-ILD (idiopathic pulmonary fibrosis (IPF), n=64; non-IPF, n=103). Antifibrotics improved the FVC decline in both IPF (p=0.002) and non-IPF (p=0.05) (IPW: IPF, p=0.015; non-IPF, p=0.031). Among patients with IPF, OS was longer in the antifibrotic group (log-rank p=0.001). However, among patients with non-IPF, OS was not longer in the antifibrotic group (p=0.3263) (IPW and statistical matching: IPF, p=0.0534 and p=0.0018; non-IPF, p=0.5663 and p=0.5618).ConclusionThis is the first real-world study to show that antifibrotics improve the FVC decline in PF-ILD. However, among patients with non-IPF, we found no significant difference in mortality between those with and without antifibrotics. Future studies must clarify whether antifibrotics improve the prognosis of non-IPF.
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Bos, Saskia, Laurens J. De Sadeleer, Arno Vanstapel, Hanne Beeckmans, Annelore Sacreas, Jonas Yserbyt, Wim A. Wuyts, and Robin Vos. "Antifibrotic drugs in lung transplantation and chronic lung allograft dysfunction: a review." European Respiratory Review 30, no. 160 (June 1, 2021): 210050. http://dx.doi.org/10.1183/16000617.0050-2021.

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This review aims to provide an overview of pre-transplant antifibrotic therapy on peri-transplant outcomes and to address the possible role of antifibrotics in lung transplant recipients with chronic lung allograft dysfunction.Lung transplantation is an established treatment modality for patients with various end-stage lung diseases, of which idiopathic pulmonary fibrosis and other progressive fibrosing interstitial lung diseases are growing indications. Theoretically, widespread use of antifibrotics prior to lung transplantation may increase the risk of bronchial anastomotic complications and impaired wound healing.Long-term graft and patient survival are still hampered by development of chronic lung allograft dysfunction, on which antifibrotics may have a beneficial impact.Antifibrotics until the moment of lung transplantation proved to be safe, without increasing peri-transplant complications. Currently, best practice is to continue antifibrotics until time of transplantation. In a large multicentre randomised trial, pirfenidone did not appear to have a beneficial effect on lung function decline in established bronchiolitis obliterans syndrome. The results of antifibrotic therapy in restrictive allograft syndrome are eagerly awaited, but nonrandomised data from small case reports/series are promising.
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Soskis, Alyssa, and Robert Hallowell. "Antifibrotic Therapy: Is There a Role in Myositis-Interstitial Lung Disease?" Respiration 100, no. 9 (2021): 923–32. http://dx.doi.org/10.1159/000515607.

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Interstitial lung disease (ILD) is a cause of substantial morbidity and mortality amongst autoimmune diseases, including myositis. Despite first-line therapy with immunosuppression, many inflammatory ILDs advance to a fibrotic stage. In such patients, progressive fibrosis may be amenable to treatment with antifibrotic medications, which were initially studied and approved for the treatment of idiopathic pulmonary fibrosis. We here review the available data that support the use of antifibrotics in connective tissue diseases and progressive fibrosing ILDs. There is now a growing body of evidence in both large randomized clinical trials and on the evolving pathophysiologic pathways to support the use of antifibrotics in select patients with autoimmune ILD and a fibrotic phenotype. Further study of antifibrotics in combination with immunosuppressive medications, and in the myositis-ILD population, is needed.
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Jegal, Yangjin, Jong Sun Park, Song Yee Kim, Hongseok Yoo, Sung Hwan Jeong, Jin Woo Song, Jae Ha Lee, et al. "Clinical Features, Diagnosis, Management, and Outcomes of Idiopathic Pulmonary Fibrosis in Korea: Analysis of the Korea IPF Cohort (KICO) Registry." Tuberculosis and Respiratory Diseases 85, no. 2 (April 1, 2022): 185–94. http://dx.doi.org/10.4046/trd.2021.0123.

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Background: The Korea Interstitial Lung Disease Study Group has made a new nationwide idiopathic pulmonary fibrosis (IPF) registry because the routine clinical practice has changed due to new guidelines and newly developed antifibrotic agents in the recent decade. The aim of this study was to describe recent clinical characteristics of Korean IPF patients.Methods: Both newly diagnosed and following IPF patients diagnosed after the previous registry in 2008 were enrolled. Survival analysis was only conducted for patients diagnosed with IPF after 2016 because antifibrotic agents started to be covered by medical insurance of Korea in October 2015.Results: A total of 2,139 patients were analyzed. Their mean age at diagnosis was 67.4±9.3 years. Of these patients, 76.1% were males, 71.0% were ever-smokers, 14.4% were asymptomatic at the time of diagnosis, and 56.9% were at gender-agephysiology stage I. Occupational toxic material exposure was reported in 534 patients. The mean forced vital capacity was 74.6% and the diffusing capacity for carbon monoxide was 63.6%. Treatment with pirfenidone was increased over time: 62.4% of IPF patients were treated with pirfenidone initially. And 79.2% of patients were treated with antifiboritics for more than three months during the course of the disease since 2016. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.Conclusion: In the recent Korean IPF registry, the percentage of IPF patients treated with antifibrotics was increased compared to that in the previous IPF registry. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.
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Caliskan, Canay, Benjamin Seeliger, Benedikt Jäger, Jan Fuge, Tobias Welte, Oliver Terwolbeck, Julia Freise, Coline H. M. van Moorsel, Yingze Zhang, and Antje Prasse. "Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis—Part B." Journal of Clinical Medicine 9, no. 6 (June 25, 2020): 1993. http://dx.doi.org/10.3390/jcm9061993.

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Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality. CC-chemokine ligand 18 (CCL18) is predictive of survival in IPF. We described correlation of CCL18 serum levels with the genotype of rs2015086 C > T polymorphism the CCL18-gene, which was associated with survival in a pre-antifibrotic cohort (Part-A). Herein (Part-B), we aimed to validate these findings and to study the effects of antifibrotics. Two cohorts were prospectively recruited, cohort-A (n = 61, pre-antifibrotic) and cohort B (n = 101, received antifibrotics). Baseline CCL18 serum level measurement by enzyme-linked immunosorbent assay (ELISA, serially in cohort B) and genotyping of rs2015086 was performed and correlated with clinical outcomes. The CT genotype was present in 15% and 31% of patients. These patients had higher CCL18 levels compared to the TT-genotype (cohort-A: 234 vs. 115.8 ng/mL, p < 0.001; cohort B: 159.5 vs. 120 ng/mL, p = 0.0001). During antifibrotic therapy, CCL18 increased (p = 0.0036) regardless of rs2015086-genotype and antifibrotic-agent. In cohort-A, baseline CCL18-cutoff (>120 ng/mL) and CT-genotype were associated with mortality (p = 0.041 and p = 0.0051). In cohort-B, the CCL18-cutoff (>140 ng/mL) was associated with mortality (p = 0.003) and progression (p = 0.004), but not the CT/CC-genotype. In conclusion, we validated the correlation between rs2015086-genotype and CCL18 serum levels, which was predictive of (progression-free)-survival in two prospective validation cohorts.
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Dhar, Raja. "Antifibrotics in India." Lung India 36, no. 5 (2019): 445. http://dx.doi.org/10.4103/lungindia.lungindia_379_19.

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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.
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Boleto, Gonçalo, Jérôme Avouac, and Yannick Allanore. "The role of antifibrotic therapies in the treatment of systemic sclerosis–associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2110666. http://dx.doi.org/10.1177/1759720x211066686.

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Systemic sclerosis (SSc) is a rare autoimmune condition with complex pathogenesis characterized by a heterogeneous presentation and different disease courses. Fibrosis of multiple organs including the lungs favored by inflammation and vasculopathy is the hallmark of SSc. SSc-associated interstitial lung disease (SSc-ILD) is common and can be associated with poor outcomes, this complication being the leading cause of death in recent series. Because of its huge heterogeneity, SSc-ILD management can be very challenging. Immunosuppressive therapy has long been used to prevent SSc-ILD progression with modest effects in clinical trials. However, thanks to a better understating of SSc pathogenesis, innovative therapies including antifibrotics are increasingly being developed. The achievement of the Safety and Efficacy of Nintedanib in Systemic SClerosIS (SENSCIS) trial has led to the approval by drug agencies of the first antifibrotic drug for SSc-ILD. In parallel, other antifibrotics are being investigated as possible beneficial therapies in SSc-ILD. An important unmet need remains to clarify the positioning of the various strategies, such as the added value of combination of immunosuppressants and antifibrotic therapies in patients at high risk of progression. Indeed, irreversible lung injury or self-perpetuated progression highlights the concept of a window of opportunity in SSc-ILD patients. Herewith, we provide an overview of the most significant clinical trials with antifibrotic drugs developed in recent years for the management of SSc-ILD and a viewpoint about their positioning in treatment algorithms.
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Cohen-Naftaly, Michal, and Scott L. Friedman. "Current status of novel antifibrotic therapies in patients with chronic liver disease." Therapeutic Advances in Gastroenterology 4, no. 6 (July 22, 2011): 391–417. http://dx.doi.org/10.1177/1756283x11413002.

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Fibrosis accumulation is a dynamic process resulting from a wound-healing response to acute or chronic liver injury of all causes. The cascade starts with hepatocyte necrosis and apoptosis, which instigate inflammatory signaling by chemokines and cytokines, recruitment of immune cell populations, and activation of fibrogenic cells, culminating in the deposition of extracellular matrix. These key elements, along with pathways of transcriptional and epigenetic regulation, represent fertile therapeutic targets. New therapies include drugs specifically designed as antifibrotics, as well as drugs already available with well-established safety profiles, whose mechanism of action may also be antifibrotic. At the same time, the development of noninvasive fibrogenic markers, and techniques (e.g. fibroscan), as well as combined scoring systems incorporating serum and clinical features will allow improved assessment of therapy response. In aggregate, the advances in the elucidation of the biology of fibrosis, combined with improved technologies for assessment will provide a comprehensive framework for design of antifibrotics and their analysis in well-designed clinical trials. These efforts may ultimately yield success in halting the progression of, or reversing, liver fibrosis.
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Tzilas, Vasilios, Argyris Tzouvelekis, Evangelos Bouros, Theodoros Karampitsakos, Maria Ntassiou, Eleni Avdoula, Athena Trachalaki, Katerina Antoniou, Ganesh Raghu, and Demosthenes Bouros. "Clinical experience with antifibrotics in fibrotic hypersensitivity pneumonitis: a 3-year real-life observational study." ERJ Open Research 6, no. 4 (October 2020): 00152–2020. http://dx.doi.org/10.1183/23120541.00152-2020.

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BackgroundFibrotic hypersensitivity pneumonitis (f-HP) can exhibit a progressive course similar to idiopathic pulmonary fibrosis (IPF). The lack of diagnostic guidelines and randomised controlled trials in this population represent a significant unmet need.ObjectivesTo describe our clinical experience with antifibrotics in patients with f-HP.Material and methodsRetrospective study of 30 patients diagnosed with f-HP upon re-evaluation within a multidisciplinary team discussion of 295 consecutive patients (January 2012 to December 2017) who had been diagnosed initially with IPF at outside facilities and were referred to our centres.ResultsPirfenidone was initially administered to 14 (46.7%) patients and nintedanib to 16 (53.3%) patients. There were 26 (86.7%) males, with mean±sd age 70.2±8.4 years. The annual rate of decline in forced vital capacity (FVC) % predicted over the 3-year treatment period adjusted for baseline FVC % pred measurement was 4.2% (95% CI 1.9–6.6%, p=0.001) and 7.5% (95% CI 3.3–11.7%; p=0.001) in imputation analysis. The annual rate of decline in diffusing capacity of the lung for carbon monoxide (DLCO) % predicted throughout the 3-year treatment period adjusted for baseline DLCO % pred was 5.7% (95% CI 3.1–8.4%, p<0.001) and 5.8% (95% CI 3.4–8.1%, p<0.001) in imputation analysis. The nature of adverse events was related to the type of antifibrotic agent administered.ConclusionIn patients with f-HP receiving antifibrotics there is a statistically significant annual decline in FVC % pred and DLCO % pred over a period of 3 years. Prospective randomised trials exceeding 1 year are warranted to determine the long-term efficacy of antifibrotics.
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Dissertations / Theses on the topic "Antifibrotics"

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Venalis, Paulius. "The performance of antifibrotic agents in preclinical models of systemic sclerosis." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2010. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2010~D_20101001_150819-57019.

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Systemic sclerosis (SSc) – is one of the most complicated and fatal systemic diseases, and the lack of effective therapy is very evident. The tyrosine kinase inhibitor imatinib mesylate (IM) was shown to inhibit TGF-β and PDGF signaling pathways and prevent the development of dermal fibrosis upon challenge with bleomycin in murine model of SSc. The aim of therapy is not only to stop disease progression, but even induce regression of preexisting fibrosis. On other hand, blocking TGF-β and PDGF signaling in angiogenesis might worsen the vascular manifestations of SSc. We found important to evaluate effectiveness of IM for the treatment of pre-established tissue fibrosis and to exclude that the anti-fibrotic effects of IM are complicated by inhibitory effects on endothelial cell functions. Aim of the study: assess the effect of IM on the process of fibrosis and endothelium in experimental models of systemic sclerosis and cell cultures. Objectives of the study: assess the effectiveness of IM on murine models of established fibrosis; evaluate if IM has an effect on basal functions of endothelial cells; assess effect of IM on the process of angiogenesis. We have shown that IM exerts potent antifibrotic effects in two different models of SSc. Imatinib was effective for prevention of fibrosis and for treatment of established dermal fibrosis. We’ve demonstrated that IM does not inhibit major functions of endothelial cells. Thus, IM might not augment further the preexisting vascular... [to full text]
Sisteminė sklerozė (SSc) – viena sunkiausių ir fatališkiausių autoimuninių sisteminių reumatinių ligų, o bazinių vaistų stygius, šiai ligai gydyti, itin didelis. Į onkologinę klinikinę praktiką įdiegtas tirozinkinazių inhibitorius – imatinibo mezilatas(IM). IM blokuoja TGF-β ir PDGF intraląstelinio signalo perdavimą ir taip sąlygoja fibrozės prevenciją SSc pelių modelyje. Mums buvo svarbu išsiaiškinti, ar imatinibas gali turėti įtakos ne tik prevencijai, bet ir susiformavusiai fibrozei. Be to TGF-β ir PDGF blokavimas angiogenezėje, galėtų riboti daug žadančio fibrozės inhibitoriaus IM naudojimą gydant SSc. Darbo tikslas: įvertinti imatinibo mezilato poveikį fibrozės procesui ir endoteliui sisteminės sklerozės eksperimentiniuose modeliuose ir ląstelių kultūrose. Darbo uždaviniai: įvertinti imatinibo efektyvumą neuždegiminiame SSc modelyje ir patikrinti imatinibo mezilato efektyvumą uždegiminiame suformuotos fibrozės modelyje; ištirti, ar terapinės imatinibo mezilato koncentracijos daro neigiamą poveikį gyvybinėms endotelio funkcijoms; įvertinti imatinibo mezilato poveikį angiogenezės etapams. Mūsų gauti duomenys rodo, kad: IM ne tik sustabdė bet ir paskatino jau egzistuojančios (bleomicino sukeltos) odos firbrozės regresiją; IM ryškiai sumažino poodžio ir odos storį, bei normalizavo miofibroblastų skaičių Tsk-1 pelėse; IM neturėjo poveikio endotelio ląstelių bazinėms funkcijoms; IM neturėjo neigiamo poveikio angiogenezės etapams.
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Gerarduzzi, Casimiro. "The phosphoproteome network of the PGE2/EP axis: Extrapolation towards an Antifibrotic Machinery." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110368.

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Fibrosis is a complex chronic disease characterized by a persistent repair response. Its pathogenesis is poorly understood but it is known to require the activity of TGFbeta and extracellular matrix (ECM) tension, both of which drive fibroblasts to transition into a myofibroblast phenotype (FMT). As the effector cells of repair, myofibroblasts migrate to the site of injury to deposit excessive amounts of type I collagen as well as other matrix proteins and stimulate high levels of contraction. Such actions are vital for wound closure and re-establishing the normal tissue structure however, limit normal tissue repair and remodeling when left uncontrolled. The cellular and molecular mechanisms regulating fibrosis are not well defined but hallmarks of the myofibroblast phenotype include major cytoskeletal rearrangements, formation of alpha-smooth muscle actin (alpha-sma)-rich stress fibers, and mature focal adhesions (FAs). Prominent signalling pathways that support myofibroblastic differentiation include TGFβ-dependent signalling, Wnt/beta-catenin, Ras/Raf/MAP kinase and Rho-Associated Kinase (ROCK)-dependent pathways. Resolution of the myofibroblast phenotype is vital to prevent continual wound repair, otherwise further deposition of ECM proteins substantiate tissue fibrosis. It is well known that PGE2 inhibits human FMT through mechanisms that are vaguely known. Our laboratory has created a strategy to better understand the signalling pathways in which the antifibrotic mediator PGE2 prevents myofibroblast development. Our work describes a draft of the complete PGE2-dependent phosphoproteome/GalphaS signalosome in fibroblast-like cell phenotypes (by PhosphoScanTM, Cell Signalling), which include proteins associated with cellular differentiation and cytoskeletal/adhesion structure. Furthermore, we have identified the specific amino acid sequence of novel phosphorylation sites, vital information towards the control process of a protein's activity. Examples of PGE2-induced phosphoproteins associated with myofibroblastic activities include beta-catenin (differentiation), RIN1 (Ras-inhibitor) (migration), ROCK2 (contraction), as well as various proteins upstream and downstream of ROCK. Giving weight to our strategy, mutational analysis of the ROCK2 serine 1379 phosphosite prevented PGE2 inhibition of the enzyme, potentially inhibiting myofibroblast contraction. Furthermore, mutation of the RIN1 serine 291 and 292 phosphosites prevented the inhibition of PGE2 on TGFβ induced migration, another vital characteristic of myofibroblasts. Other observations included a marked reversal of cytoskeletal protein phosphorylation, loss of stress fiber/FA formation, suppression of alpha smooth muscle actin (alpha-sma) expression, and blockade of the FMT through activation of the "phospholipase/cyclooxygenase/mPGE synthase/prostaglandin E2 biosynthetic axis" in human fibroblasts. Ultimately, the results will encourage PGE2 mimetics as potential therapeutics for the treatment of fibrosis.
La fibrose est une maladie chronique complexe caractérisée par une réaction de réparation persistante. Sa pathogénie est mal comprise mais on la connaît pour exiger l'activité de TGFbeta et une tension extracellulaire de la matrice (ECM), qui dirige des fibroblastes dans une transition vers un phénotype de myofibroblast (FMT). Comme cellules effectrices de la réparation, les myofibroblasts migrent au site des dommages pour déposer des quantités excessives de collagène de type I aussi bien que d'autres protéines de matrice et pour stimuler de hauts niveaux de contraction. De telles actions sont essentielles pour la fermeture de blessure et le rétablissement de la structure normale du tissu cependant, laissé incontrôlé elle limite la réparation normale et le remodelage du tissu. Les mécanismes cellulaires et moléculaires réglant la fibrose ne sont pas bien définis mais les marqueurs du phénotype de myofibroblastes incluent des réarrangements cytosquelettiques importants, la formation des fibres de stress riches en alpha-actine du muscle lisses (alpha-sma), et des adhérences focales (FAs). Les voies importantes de signalisation qui soutiennent la différenciation myofibroblastique incluent une signalisation TGFbeta-dépendante, la Wnt/beta-catenin, la kinase de Ras/Raf/MAP et les voies dépendantes de la kinase Rho-Associée (ROCK). La résolution du phénotype de myofibroblast est essentielle pour empêcher la réparation continuelle de la blessure, autrement davantage de dépôt des protéines extracellulaire de la matrice explique la fibrose du tissu. Il est bien connu que la PGE2 empêche FMT humain par des mécanismes qui sont vaguement connus. Notre laboratoire a créé une stratégie pour mieux comprendre les voies de signalisation dans lesquelles la PGE2, un médiateur antifibrotique , empêche le développement de myofibroblast. Notre travail décrit un croquis complet du phosphoprotéome/GalphaS signalosome dépendante de la PGE2 dans les cellules avec le phénotype fibroblaste (par PhosphoScanTM, signalisation cellulaires), qui incluent des protéines liées à la différenciation cellulaire et à la structure cytosquelettique/adhérence. En outre, nous avons identifié la séquence des acides aminés spécifique de sites inédits de phosphorylation, une information indispensable vers le procédé de contrôle de l'activité d'une protéine. Des exemples de phosphoprotéines induites par la PGE2 liées aux activités myofibroblastic incluent le beta-cateninix(différenciation), le RIN1 (Ras-inhibiteur) (migration), le ROCK2 (contraction), aussi bien que les diverses protéines en amont et en aval de la ROCK. Donnant de la considération à notre stratégie, l'analyse mutationnelle du phosphosite ROCK2 a empêché l'inhibition de l'enzyme par la PGE2, inhibant potentiellement la contraction myofibroblastique. En outre, la mutation du phosphosite RIN1 a empêché l'inhibition de la PGE2 sur la migration induite par le TGFbeta, une autre caractéristique essentielle des myofibroblasts. D'autres observations inclus une inversion marquée de la phosphorylation des protéines du cytosquelette, la perte de formation de fibre de stress et des adhérences focales, la suppression de l'expression de l'alpha-actine du muscle lisses (alpha-sma), et le blocus du FMT par l'activation « de l'axe de biosynthèse des phospholipase/cyclooxygenase/mPGE synthase/prostaglandine E2» dans les fibroblastes humains. Finalement, les résultats encourageront la PGE2 en tant que cible thérapeutique potentielle pour le traitement de la fibrose.
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Lu, Changwu [Verfasser]. "Antifibrotic drugs: new candidates for the treatment of pulmonary arterial hypertension? / Changwu Lu." Gießen : Universitätsbibliothek, 2018. http://d-nb.info/1163533688/34.

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Brook, Nicholas Roger. "Nephrotoxicity of immunosuppressant drugs in salt-depletion and modification of effect by an antifibrotic agent." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29914.

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The calcineurin inhibitors, cyclosporine and tacrolimus, are pivotal immunosuppressants in renal transplantation, but produce a cascade of acute (functional) and chronic (fibrotic) injurious events that contribute to chronic allograft nephropathy (CAN). Using the rat salt depletion model of calcineurin inhibitor toxicity, this study aimed to examine the effects of clinically relevant combinations of cyclosporine, tacrolimus and sirolimus on renal functional, structural and molecular markers of injury. Further, the effect of pirfenidone when added to these drug combinations was examined. There were differences in the effects of cyclosporine and tacrolimus on functional and molecular variables, with tacrolimus displaying more favourable results. As sole therapy, sirolimus had no effect on renal function or messenger RNA expression. Deterioration in renal function and a deleterious effect on molecular markers of fibrosis were seen when cyclosporine and sirolimus were combined at high doses; at lower doses, favourable outcomes for these end-points were elicited. When sirolimus and tacrolimus were combined, renal function worsened and the beneficial molecular effects of tacrolimus were reversed. Pirfenidone's actions were non-dose dependent and beneficial effects for renal function and molecular markers were demonstrated. The effect of pirfenidone on renal function has not previously been described. There were no differences in urinary protein or interstitial fibrosis measurements across the groups. Without fibrosis, it is impossible to say whether pirfenidone acted in a truly antifibrotic manner. However, the molecular changes possibly represent interim markers of fibrosis, suggesting such an effect may have been developing.
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Finato, Angela Carolina. "Avaliação de terapias antifibróticas associadas aos antifúngicos itraconazol e cotrimoxazol em modelo murino de paracoccidioidomicose pulmonar." Botucatu, 2017. http://hdl.handle.net/11449/151468.

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Orientador: James Venturini
Resumo: Paracoccidioidomicose (PCM) é uma micose sistêmica causada por fungos do gênero Paracoccidioides; suas principais formas clínicas são aguda/subaguda, crônica e residual. A PCM é uma doença restrita a países da América Latina com maior incidência no Brasil, especialmente entre os trabalhadores rurais. A maioria dos pacientes com a forma crônica da doença, mesmo após tratamento eficaz, apresentam sequelas, incluindo fibrose pulmonar e adrenal. Os problemas sociais, econômicos e psicológicos desencadeados pela fibrose pulmonar são subestimados; além disso, a fibrose na PCM permanece negligenciada, uma vez que não há tratamento. Dessa forma, o estudo teve por objetivo investigar a influência de drogas com potencial antifibrótico (pentoxifilina - PTX, azitromicina - AZT e talidomida - Thal) associadas aos tratamentos antifúngicos com itraconazol - ITC e cotrimoxazol - CMX em modelo murino de PCM pulmonar. Para tanto, camundongos BALB/c machos foram inoculados com leveduras do isolado 326 de P. brasiliensis e após 8 semanas de infecção foi dado início aos esquemas terapêuticos: PTX/ITC, PTX/CMX, AZT/ITC, AZT/CMX, Thal/ITC e Thal/CMX. Após 8 semanas de tratamento, os animais foram eutanasiados a fim de se avaliar a deposição de fibras colágenas, produção de hidroxiprolina, recuperação de fungos viáveis e a porcentagem das áreas com lesão nos pulmões e peso corporal. Visando identificar os mecanismos envolvidos foi avaliada a produção de TGF-β1, CCL3, IFN-γ, TNF-α, IL-10, VEGF, IL-6,... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Paracoccidioidomycosis (PCM) is a systemic mycosis caused by fungi of Paracoccidioides genus; the main clinical forms are acute/subacute, chronic and residual. PCM is a disease restricted to Latin American countries with a higher incidence in Brazil, especially among rural workers. Most patients with the chronic form, even after effective treatment, present sequelae, including pulmonary and adrenal fibrosis. The social, economic and psychological problems triggered by pulmonary sequels are underestimated. In addition, fibrosis in PCM remains neglected, since there is no treatment. The aim of this study was to investigate the influence of antifibrotic drugs (pentoxifylline - PTX, azithromycin - AZT and thalidomide - Thal) associated with antifungal treatments with itraconazole - ITC and cotrimoxazole - CMX in a murine model of pulmonary PCM. Male BALB/c mice were inoculated with P. brasiliensis “isolated 326” and after 8 weeks of infection the treatment were started: PTX/ITC, PTX/CMX, AZT/ITC, AZT/CMX, Thal/ITC and Thal/CMX. After 8 weeks of treatment, the mice were euthanized in order to evaluate the deposition of collagen fibers, hydroxyproline production, recovery of viable fungi and the percentage of areas with injury in lung and body weight. In order to identify the mechanisms involved, the production of TGF-β1, CCL3, IFN-γ, TNF-α, IL-10, VEGF, IL-6, IL-1β, IL-17 and IL-2 in the lung homogenate was evaluated. Our findings revealed that infected mice treated with PTX/ITC s... (Complete abstract click electronic access below)
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Arias-Kuhn, Mónica S. "Antifibrotic therapy in the liver by adenovirus mediated expression of a TGF [beta]1 [beta 1] antisense mRNA /." Aachen : Shaker, 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=013111065&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Arias-Kuhn, Mónica S. [Verfasser]. "Antifibrotic Therapy in the Liver by Adenovirus-mediated Expression of a TGF-beta1 Antisense mRNA / Mónica S Arias-Kuhn." Aachen : Shaker, 2004. http://d-nb.info/1181604060/34.

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Öcal, Sinan [Verfasser], Ulrich [Gutachter] Baumann, and Karsten [Gutachter] Niefind. "The HSP47 - Procollagen Interaction: Mechanism of pH-Dependent Client Release and Development of Antifibrotic Inhibitors / Sinan Öcal ; Gutachter: Ulrich Baumann, Karsten Niefind." Köln : Universitäts- und Stadtbibliothek Köln, 2017. http://d-nb.info/117241467X/34.

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Kaps, Leonard [Verfasser]. "In vivo gene silencing in the liver with siRNA loaded non-biodegradable and biodegradable cationic nanohydrogel particles for antifibrotic therapy / Leonard Kaps." Mainz : Universitätsbibliothek Mainz, 2018. http://d-nb.info/1152103210/34.

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Matei, Alexandru-Emil [Verfasser], Jörg [Akademischer Betreuer] Distler, Jörg [Gutachter] Distler, and Georg [Gutachter] Schett. "Protein kinases G as downstream mediators of the antifibrotic effects of stimulators of soluble guanylate cyclase / Alexandru-Emil Matei ; Gutachter: Jörg Distler, Georg Schett ; Betreuer: Jörg Distler." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2019. http://d-nb.info/1202608485/34.

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Books on the topic "Antifibrotics"

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Nanomedicine - Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier, 2012. http://dx.doi.org/10.1016/c2011-0-04217-5.

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Nanomedicine: Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier Science & Technology Books, 2012.

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Duzgunes, Nejat. Nanomedicine: Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier Science & Technology Books, 2012.

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Book chapters on the topic "Antifibrotics"

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Pinzani, Massimo. "Antifibrotic Drugs." In Portal Hypertension V, 211–17. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444393989.ch21.

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Thuy, Le Thi Thanh, Hoang Hai, Vu Ngoc Hieu, Ninh Quoc Dat, Dinh Viet Hoang, and Norifumi Kawada. "Antifibrotic Therapy for Liver Cirrhosis." In The Evolving Landscape of Liver Cirrhosis Management, 167–89. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7979-6_15.

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Handa, Tomohiro, and Arata Azuma. "Pharmacotherapy of IPF Using Antifibrotic Compounds." In Idiopathic Pulmonary Fibrosis, 147–59. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_9.

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Zhang, Ying-Ying, Ying Yu, and Chen Yu. "Antifibrotic Roles of RAAS Blockers: Update." In Advances in Experimental Medicine and Biology, 671–91. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_33.

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Esmat, Gamal, and Maissa El Raziky. "Changing outcomes with antiviral or antifibrotic therapies." In Cirrhosis: A practical guide to management, 274–82. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118412640.ch24.

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Menke, A., R. Vogelmann, M. Bachem, and G. Adler. "Mechanisms of Fibrosis and Potential Antifibrotic Agents." In Pancreatic Disease, 132–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60068-5_13.

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Cordeiro, M. Francesca, Annelie Maass, Clive Migdal, and Li Guo. "TGF-β-Related Antifibrotic Strategies in the Eye." In Transforming Growth Factor-β in Cancer Therapy, Volume I, 663–73. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-292-2_42.

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Schuppan, Detlef, Jae Jin Cho, Masahiko Koda, and Eckhart G. Hahn. "Lecture - Antifibrotic Therapy: Future Cure for Portal Hypertension?" In Portal Hypertension III: Proceedings of the Third Baverno International Consensus Workshop on Definitions, Methodology and Therapeutic Strategies, 112–26. Oxford, UK: Blackwell Science Ltd, 2008. http://dx.doi.org/10.1002/9780470760154.ch8.

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Lupher Jr., Mark L., and W. Scott Willett. "Serum amyloid P: A novel antifibrotic agent with therapeutic potential." In New Drugs and Targets for Asthma and COPD, 261–66. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320829.

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Mathew, Anna, Robyn Cunard, and Kumar Sharma. "Antifibrotic Treatment and Other New Strategies for Improving Renal Outcomes." In Contributions to Nephrology, 217–27. Basel: KARGER, 2011. http://dx.doi.org/10.1159/000325671.

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Conference papers on the topic "Antifibrotics"

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Muñoz Burgos, M., M. Mejias Trueba, and T. Desongles Corrales. "4CPS-123 Antifibrotics in idiopathic pulmonary fibrosis management: pirfenidone and nintedanib." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.272.

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Sand, Jannie, Natasja Gudmann, Sarah Rønnow, Sarah Brockbank, Simon Cruwys, Morten Karsdal, and Diana Leeming. "Scar-in-a-Jar, an in vitro screening tool for antifibrotics." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa597.

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Porse, Simon, Nils Hoyer, Thomas Skovhus Prior, Elisabeth Bendstrup, and Saher B. Shaker. "Prognostic significance of dose reduction of antifibrotics in patients with IPF." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa1204.

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Llanos-González, Ana Belén, Sara García Gil, Juan Alfonso Bonilla Arjona, Sonia García Hernández, Verónica S. Hernández García, Paula Pérez De Armas, Nelson Mesa León, and Orlando Acosta Fernández. "Experience with antifibrotics treatment in progressive interstitial lung diseases non-IPF." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2375.

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Huong, YK, V. Dhunnoo, C. Leonard, R. Venkateswaran, and N. Chaudhuri. "M24 Do antifibrotics impact on lung transplantation outcomes in idiopathic pulmonary fibrosis?" In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.446.

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Bhomra, PS, GA Burge, AM Turner, PS Burge, and GI Walters. "P158 Which factors predict early discontinuation of antifibrotics in idiopathic pulmonary fibrosis?" In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.316.

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Ryan, J., K. Malcolm, E. D. Farrand, N. A. Kolaitis, B. J. Ley, J. K. Brown, and J. R. Greenland. "Medication Discontinuation and Survival in Elderly Veterans on Antifibrotics for Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4761.

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Naqvi, M., and A. West. "P138 Review of patient longevity when managed with antifibrotics for idiopathic pulmonary fibrosis." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.283.

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Tzilas, Vasilios, Argyrios Tzouvelekis, Evangelos Bouros, Theodoros Karampitsakos, Maria Ntassiou, Eleni Avdoula, Athina Trachalaki, Katerina Antoniou, and Demosthenes Bouros. "Efficacy of antifibrotics in chronic hypersensitivity pneumonitis. A 3 year real-life observational study." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.737.

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Adams, C., S. Shapera, C. J. Ryerson, P. Wilcox, T. M. To, M. Sadatsafavi, J. Morisset, et al. "'Real World' Therapeutic Approach and Associations with FVC Decline in IPF Patients Treated with Antifibrotics." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1504.

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