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Journal articles on the topic 'Fibrosis regression'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Landge, Karishma, Vineeta Ojha, KartikP Ganga, Prateek Kaushik, Pooja Sharma, Priya Jagia, Sudheer Arava, et al. "Endomyocardial fibrosis regression." Journal of the Practice of Cardiovascular Sciences 5, no. 2 (2019): 102. http://dx.doi.org/10.4103/jpcs.jpcs_7_19.

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2

Iredale, John, and Lara Campana. "Regression of Liver Fibrosis." Seminars in Liver Disease 37, no. 01 (February 15, 2017): 001–10. http://dx.doi.org/10.1055/s-0036-1597816.

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3

Andrade, Zilton A. "Schistosomiasis and hepatic fibrosis regression." Acta Tropica 108, no. 2-3 (November 2008): 79–82. http://dx.doi.org/10.1016/j.actatropica.2008.04.003.

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4

Sato, Masaaki, David M. Hwang, Zehong Guan, Jonathan C. Yeung, Masaki Anraku, Dirk Wagnetz, Shin Hirayama, Thomas K. Waddell, Mingyao Liu, and Shaf Keshavjee. "Regression of Allograft Airway Fibrosis." American Journal of Pathology 179, no. 3 (September 2011): 1287–300. http://dx.doi.org/10.1016/j.ajpath.2011.05.032.

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5

Saffioti, Francesca, and Massimo Pinzani. "Development and Regression of Cirrhosis." Digestive Diseases 34, no. 4 (2016): 374–81. http://dx.doi.org/10.1159/000444550.

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Liver cirrhosis is the ultimate consequence of the wound healing reaction subsequent to a chronic injury, which leads to a complete derangement of the normal hepatic lobular and vascular architecture. Cirrhosis is characterized by patterns of evolution depending on the causative agent and a series of complex underlining mechanisms in which neo-angiogenesis and necro-inflammation play a key role. The importance of the different cell types involved and of the extracellular matrix composition as well as the role of innate immunity, bacterial translocation and oxidative stress are also emerging. A variable degree of regression of fibrosis and even cirrhosis has been described, in experimental models, after suspension of the liver disease causative agent. As some individual features influence the rate of fibrosis progression, genetic and epigenetic factors are likely to influence fibrosis regression. Key Messages: There is increasing awareness that cirrhosis is not a static condition but a dynamic process. Current semi-quantitative scores and clinical classifications are inaccurate and unable to identify the different phases of evolution of the advanced stages of chronic liver diseases (CLDs). The increasing availability of effective etiology-driven therapeutic options for CLDs makes reversion of cirrhosis a more possible prospective. However, the removal of the causing agent, depending on the stage of the disease, does not necessarily eliminate the risk of disease progression, decompensation and development of hepatocellular carcinoma. Also, the non-invasive markers currently validated for the assessment of fibrosis are not suitable for an effective evaluation of fibrosis regression. Conclusions: There is a critical need of a system that would be able to more accurately describe the dynamic development of cirrhosis and the impact of tissue fibrosis, neo-angiogenesis, necro-inflammation and attempted regeneration on its evolution. Effective treatment of CLD can lead to a variable degree of fibrosis regression. New markers able to evaluate this process will need to be detected and validated.

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Caligiuri, Alessandra, Alessandra Gentilini, Mirella Pastore, Stefano Gitto, and Fabio Marra. "Cellular and Molecular Mechanisms Underlying Liver Fibrosis Regression." Cells 10, no. 10 (October 15, 2021): 2759. http://dx.doi.org/10.3390/cells10102759.

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Chronic liver injury of different etiologies may result in hepatic fibrosis, a scar formation process consisting in altered deposition of extracellular matrix. Progression of fibrosis can lead to impaired liver architecture and function, resulting in cirrhosis and organ failure. Although fibrosis was previous thought to be an irreversible process, recent evidence convincingly demonstrated resolution of fibrosis in different organs when the cause of injury is removed. In the liver, due to its high regenerative ability, the extent of fibrosis regression and reversion to normal architecture is higher than in other tissues, even in advanced disease. The mechanisms of liver fibrosis resolution can be recapitulated in the following main points: removal of injurious factors causing chronic hepatic damage, elimination, or inactivation of myofibroblasts (through various cell fates, including apoptosis, senescence, and reprogramming), inactivation of inflammatory response and induction of anti-inflammatory/restorative pathways, and degradation of extracellular matrix. In this review, we will discuss the major cellular and molecular mechanisms underlying the regression of fibrosis/cirrhosis and the potential therapeutic approaches aimed at reversing the fibrogenic process.

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7

Chen, Li, David A. Brenner, and Tatiana Kisseleva. "Combatting Fibrosis: Exosome‐Based Therapies in the Regression of Liver Fibrosis." Hepatology Communications 3, no. 2 (December 13, 2018): 180–92. http://dx.doi.org/10.1002/hep4.1290.

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8

Elsharkawy, Aisha, Reham Samir, and Mohamed El-Kassas. "Fibrosis regression following hepatitis C antiviral therapy." World Journal of Hepatology 14, no. 6 (June 27, 2022): 1120–30. http://dx.doi.org/10.4254/wjh.v14.i6.1120.

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9

ZOIS, C. D., G. H. BALTAYIANNIS, P. KARAYIANNIS, and E. V. TSIANOS. "Systematic review: hepatic fibrosis - regression with therapy." Alimentary Pharmacology & Therapeutics 28, no. 10 (November 2008): 1175–87. http://dx.doi.org/10.1111/j.1365-2036.2008.03840.x.

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10

Amital, H. "Fibrosis regression induced by intravenous gammaglobulin treatment." Annals of the Rheumatic Diseases 62, no. 2 (February 1, 2003): 175–77. http://dx.doi.org/10.1136/ard.62.2.175.

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11

Bourlière, M., A. Kahloun, and G. Gascou-Tessonnier. "Analogs and fibrosis regression in hepatitis B." Gastroentérologie Clinique et Biologique 33, no. 10-11 (October 2009): 923–29. http://dx.doi.org/10.1016/j.gcb.2009.06.003.

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12

Akarca, U. S. "Analogs and fibrosis regression in hepatitis B." Gastroentérologie Clinique et Biologique 34, no. 6-7 (August 2010): 419. http://dx.doi.org/10.1016/j.gcb.2010.03.010.

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13

&NA;. "Regression of myocardial fibrosis seen with lisinopril." Inpharma Weekly &NA;, no. 1259 (October 2000): 19. http://dx.doi.org/10.2165/00128413-200012590-00051.

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14

Sood, Vikrant, Bikrant Bihari Lal, Archana Rastogi, Rajeev Khanna, Dinesh Rawat, and Seema Alam. "Regression of fibrosis in pediatric liver diseases." Indian Journal of Gastroenterology 37, no. 3 (May 2018): 266–70. http://dx.doi.org/10.1007/s12664-018-0847-8.

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15

Magdaleno, Fernando, and Jonel Trebicka. "Selective LOXL2 inhibition: potent antifibrotic effects in ongoing fibrosis and fibrosis regression." Gut 66, no. 9 (February 28, 2017): 1540–41. http://dx.doi.org/10.1136/gutjnl-2016-313621.

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16

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

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

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17

Brown, Ashley, and Zachary Goodman. "Hepatitis B-associated fibrosis and fibrosis/cirrhosis regression with nucleoside and nucleotide analogs." Expert Review of Gastroenterology & Hepatology 6, no. 2 (April 2012): 187–98. http://dx.doi.org/10.1586/egh.12.4.

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18

Horn, Angelika, Trayana Kireva, Katrin Palumbo-Zerr, Clara Dees, Michal Tomcik, Cinzia Cordazzo, Pawel Zerr, et al. "Inhibition of hedgehog signalling prevents experimental fibrosis and induces regression of established fibrosis." Annals of the Rheumatic Diseases 71, no. 5 (March 8, 2012): 785–89. http://dx.doi.org/10.1136/annrheumdis-2011-200883.

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ObjectivesTissue fibrosis is a leading cause of death in patients with systemic sclerosis (SSc). Effective antifibrotic treatments are not available. Here, the authors investigated inhibition of hedgehog signalling by targeting Smoothened (Smo) as a novel antifibrotic approach.MethodsThe activation status of the hedgehog pathway was assessed by immunohistochemistry for Gli transcription factors and by quantification of hedgehog target genes. Hedgehog signalling was inhibited by the selective inhibitor LDE223 and by small interfering RNA against Smo in the models of bleomycin-induced dermal fibrosis and in tight-skin-1 mice.ResultsHedgehog signalling is activated in SSc and in murine models of SSc. Inhibition of Smo either by LDE223 or by small interfering RNA prevented dermal thickening, myofibroblast differentiation and accumulation of collagen upon challenge with bleomycin. Targeting Smo also exerted potent antifibrotic effects in tight-skin-1 mice and did prevent progression of fibrosis and induced regression of pre-established fibrosis.ConclusionsInhibition of hedgehog signalling exerted potent antifibrotic effects in preclinical models of SSc in both preventive and therapeutic settings. These findings might have direct translational implications because inhibitors of Smo are already available and yielded promising results in initial clinical trials.

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19

Al-Sayegh, Rola, Santia Diab, Ghewa El-Achkar, Wared Nour-Eldine, Eva Hamade, Sophie Lotersztajn, and Aida Habib. "THU-061-Statins reduces liver fibrosis progression and promotes fibrosis regression in mice." Journal of Hepatology 70, no. 1 (April 2019): e187. http://dx.doi.org/10.1016/s0618-8278(19)30342-1.

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20

Dees, Clara, Pawel Zerr, Michal Tomcik, Christian Beyer, Angelika Horn, Alfiya Akhmetshina, Katrin Palumbo, et al. "Inhibition of Notch signaling prevents experimental fibrosis and induces regression of established fibrosis." Arthritis & Rheumatism 63, no. 5 (April 27, 2011): 1396–404. http://dx.doi.org/10.1002/art.30254.

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21

Ohkoshi, Shogo, Haruka Hirono, Kazuhiko Watanabe, Katsuhiko Hasegawa, Kenya Kamimura, and Masahiko Yano. "Natural regression of fibrosis in chronic hepatitis B." World Journal of Gastroenterology 22, no. 24 (2016): 5459. http://dx.doi.org/10.3748/wjg.v22.i24.5459.

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22

Lo, Regina C., and Haeryoung Kim. "Histopathological evaluation of liver fibrosis and cirrhosis regression." Clinical and Molecular Hepatology 23, no. 4 (December 25, 2017): 302–7. http://dx.doi.org/10.3350/cmh.2017.0078.

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23

Kisseleva, Tatiana, and David A. Brenner. "Inactivation of myofibroblasts during regression of liver fibrosis." Cell Cycle 12, no. 3 (February 2013): 381–82. http://dx.doi.org/10.4161/cc.23549.

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24

Mabire, Morgane, Hegde Pushpa, Manon Allaire, Al Sayegh Rola, JingHong Wan, Emmanuel Weiss, Richard Moreau, Hélène Gilgenkrantz, De La Grange Pierre, and Sophie Lotersztajn. "Blocking MAIT cell activation accelerates liver fibrosis regression." Journal of Hepatology 73 (August 2020): S85—S86. http://dx.doi.org/10.1016/s0168-8278(20)30720-0.

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25

Ellis, Elizabeth L., and Derek A. Mann. "Clinical evidence for the regression of liver fibrosis." Journal of Hepatology 56, no. 5 (May 2012): 1171–80. http://dx.doi.org/10.1016/j.jhep.2011.09.024.

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26

Friedman, S. L. "Fibrogenic cell reversion underlies fibrosis regression in liver." Proceedings of the National Academy of Sciences 109, no. 24 (May 29, 2012): 9230–31. http://dx.doi.org/10.1073/pnas.1206645109.

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27

Kisseleva, Tatiana, and David A. Brenner. "Anti-fibrogenic strategies and the regression of fibrosis." Best Practice & Research Clinical Gastroenterology 25, no. 2 (April 2011): 305–17. http://dx.doi.org/10.1016/j.bpg.2011.02.011.

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28

Schuppan, Detlef, Rambabu Surabattula, and Xiao Yu Wang. "Determinants of fibrosis progression and regression in NASH." Journal of Hepatology 68, no. 2 (February 2018): 238–50. http://dx.doi.org/10.1016/j.jhep.2017.11.012.

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29

Mehal, Wajahat, and Uyen To. "New approaches for fibrosis regression in alcoholic cirrhosis." Hepatology International 10, no. 5 (July 26, 2016): 773–78. http://dx.doi.org/10.1007/s12072-016-9752-3.

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30

Karsdal, Morten A., Sara T. Hjuler, Yi Luo, Daniel G. K. Rasmussen, Mette J. Nielsen, Signe Holm Nielsen, Diana J. Leeming, et al. "Assessment of liver fibrosis progression and regression by a serological collagen turnover profile." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 1 (January 1, 2019): G25—G31. http://dx.doi.org/10.1152/ajpgi.00158.2018.

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There is a need for noninvasive biomarkers that can identify patients with progressive liver fibrosis and monitor response to antifibrotic therapy. An equally important need is identification of patients with spontaneous fibrosis regression, since they may not need treatment nor be included in clinical studies with fibrosis as end point. Circulating biomarkers, originating from defined fragments of the scar tissue itself, may serve as valuable tools for this aspect of precision medicine. We investigated a panel of serological collagen formation and degradation markers to identify patients likely to regress or progress in absence of a therapeutic intervention. Plasma samples from patients with moderate-stage hepatitis C receiving placebo treatment in a phase II trial of the peroxisome proliferator-activated receptor agonist farglitazar were included. The patients had matched liver biopsies at baseline and 52 wk of follow-up. Serological biomarkers of collagen formation (PRO-C3, PRO-C4, PRO-C5) and collagen degradation (C3M, C4M, and C6M) were analyzed. Logistic regression analysis including PRO-C3 and C6M identified subjects with progressive liver fibrosis with an AUROC of 0.91 ( P < 0.0001) and positive and negative predictive values (PPV/NPV) of 75.0%/88.6%. Low levels of PRO-C5 predicted a spontaneous regression phenotype, with an odds ratio of 33.8 times higher compared with patients with high levels ( P < 0.0025) with an AUROC of 0.78 ( P < 0.0001) and PPV/NPV of 60.0%/95.7%. Two collagen fragments (PRO-C3 and C6M) identified liver fibrosis progressors, and one collagen fragment (PRO-C5) identified liver fibrosis regressors. These biomarkers may improve patient stratification and monitor treatment efficacy in studies with fibrosis as clinical end point. NEW & NOTEWORTHY In this study we report two biomarkers of collagen fragments (PRO-C3 and C6M) that are able to identify liver fibrosis progressors while one biomarker (PRO-C5) identified liver fibrosis regressors. In particular, we present three noninvasive biomarkers that can be used to identify patients with progressive liver fibrosis, monitor response to antifibrotic therapy, and also identify the spontaneous liver fibrosis regression phenotype.

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31

Stoian, Marilena, and Victor Stoica. "Current Trends on Glomerulosclerosis Regression." Journal of Medicine and Life 13, no. 2 (April 2020): 116–18. http://dx.doi.org/10.25122/jml-2020-0006.

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The role of the renin-angiotensin system in hypertension and end-organ damage has long been recognized. Angiotensin l converting enzyme inhibitors are superior to other antihypertensive agents in protecting the kidney against progressive deterioration, even in normotensive persons. Likewise, angiotensin II type 1 receptor antagonists improve or even reverse glomerulosclerosis in rat animal models. These findings suggest that Angiotensin II has nonhemodynamic effects in progressive renal disease. The renin-angiotensin system is now recognized to be linked to the induction of plasminogen activator-inhibitor-1, possibly via the AT4 receptor, thus promoting both thrombosis and fibrosis. Interactions of the renin-angiotensin system with aldosterone and bradykinin may impact both blood pressure and tissue injury. The beneficial effect on renal fibrosis of inhibiting the renin-angiotensin system likely reflects the central role that angiotensin has in regulating renal function and structure by its various actions. This article explores the renin-angiotensin-aldosterone system with plasminogen activator-inhibitor-1 interaction and the potential significance of these interactions in the pathogenesis of progressive renal disease and remodeling of renal sclerosis.

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32

Soliman, Hanan, Dina Ziada, Marwa Salama, Manal Hamisa, Rehab Badawi, Nehad Hawash, Amal Selim, and Sherief Abd-Elsalam. "Predictors for Fibrosis Regression in Chronic HCV Patients after the Treatment with DAAS: Results of a Real-world Cohort Study." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 1 (January 7, 2020): 104–11. http://dx.doi.org/10.2174/1871530319666190826150344.

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Introduction: The goal of treatment of chronic hepatitis C (HCV) is viral eradication. However, obtaining histological regression is even more important, because it will reduce the overall morbidity and mortality related to cirrhosis. Introduction of direct-acting antivirals (DAAs) in HCV improves rates of sustained virologic response (SVR). However, fibrosis regression has not been extensively assessed. The aim of this study was to detect the factors affecting fibrosis regression in chronic HCV patients treated with interferon containing regimens versus interferon-free DAA regimens. Methods: This prospective observational cohort study was conducted at the Tropical Medicine and Infectious Diseases Department, Tanta University, Egypt, between October 2015 and December 2017. Transient elastography (FibroScan®) examination was performed before therapy, at SVR12, 6 months and 1 year after completing therapy for cured patients. Results: Reduction in fibrosis was reported in; 46.7% and 49.3% of patients with moderate fibrosis, and 89% and 78.7% of patients with advanced fibrosis after one year of interferon containing and interferon free DAAs regimens respectively. Using multiple regression analysis; it was found that BMI, degrees of hepatic stiffness and steatosis were related to regression of hepatic fibrosis after therapy. Conclusion: DAAs with or without interferon resulted in a significant reduction of liver fibrosis. BMI, steatosis and liver stiffness were independent factors for fibrosis regression in chronic HCV patients treated with DAAs. Further studies are needed to explore the mechanism by which steatosis affects HCV related fibrosis regression after treatment with DAAs.

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33

Yue, Zhensheng, Zijian Jiang, Bai Ruan, Juanli Duan, Ping Song, Jingjing Liu, Hua Han, and Lin Wang. "Disruption of myofibroblastic Notch signaling attenuates liver fibrosis by modulating fibrosis progression and regression." International Journal of Biological Sciences 17, no. 9 (2021): 2135–46. http://dx.doi.org/10.7150/ijbs.60056.

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34

De Socio, G., C. Cerquaglia, V. Curigliano, C. Fonnesu, M. Giovinale, E. Verrecchia, G. M. E. Marino, L. Natale, G. B. Gasbarrini, and R. Manna. "Association between Familial Mediterranean Fever and Retroperitoneal Fibrosis: Retroperitoneal Fibrosis Regression after Colchicine Therapy." International Journal of Immunopathology and Pharmacology 22, no. 2 (April 2009): 521–24. http://dx.doi.org/10.1177/039463200902200229.

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35

Wanless, Ian R., Eisuke Nakashima, and Morris Sherman. "Regression of Human Cirrhosis." Archives of Pathology & Laboratory Medicine 124, no. 11 (November 1, 2000): 1599–607. http://dx.doi.org/10.5858/2000-124-1599-rohc.

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Abstract Context.—Cirrhosis is widely regarded as being irreversible. Recent studies have demonstrated that fibrosis may decrease with time in humans and experimental animals if the disease activity becomes quiescent. The histologic appearance of regressing cirrhosis in the human has not been described in detail. Objectives.—To define histologic parameters that indicate regression of cirrhosis and to provide an interpretation of how regression occurs from a histologic point of view. Design.—A patient who underwent a series of biopsies that showed apparent regression of hepatitis B cirrhosis is presented. In addition, 52 livers removed at transplantation having cirrhosis or incomplete septal cirrhosis were graded for histologic parameters that suggest progression or regression of fibrosis. Progression parameters were steatohepatitis, inflammation, bridging necrosis, and piecemeal necrosis. The regression parameters (collectively called the hepatic repair complex) were delicate perforated septa, isolated thick collagen fibers, delicate periportal fibrous spikes, portal tract remnants, hepatic vein remnants with prolapsed hepatocytes, hepatocytes within portal tracts or splitting septa, minute regenerative nodules, and aberrant parenchymal veins. Results and Conclusions.—Regression parameters were found in all livers and were prominent in the majority. Livers with micronodular cirrhosis, macronodular cirrhosis, and incomplete septal cirrhosis demonstrate a histologic continuum. A continuum of regressive changes was also seen within individual livers. These appearances allow one to understand visually how fibrous regions of hepatic parenchyma can be returned toward a normal appearance. Many examples of incomplete septal cirrhosis could be the product of regressed cirrhosis.

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36

Chen, Chih-Wei, Christian Beyer, Jun Liu, Christiane Maier, Chun Li, Thuong Trinh-Minh, Xiaohan Xu, et al. "Pharmacological inhibition of porcupine induces regression of experimental skin fibrosis by targeting Wnt signalling." Annals of the Rheumatic Diseases 76, no. 4 (February 2, 2017): 773–78. http://dx.doi.org/10.1136/annrheumdis-2016-210294.

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ObjectivesWnt signalling has been implicated in activating a fibrogenic programme in fibroblasts in systemic sclerosis (SSc). Porcupine is an O-acyltransferase required for secretion of Wnt proteins in mammals. Here, we aimed to evaluate the antifibrotic effects of pharmacological inhibition of porcupine in preclinical models of SSc.MethodsThe porcupine inhibitor GNF6231 was evaluated in the mouse models of bleomycin-induced skin fibrosis, in tight-skin-1 mice, in murine sclerodermatous chronic-graft-versus-host disease (cGvHD) and in fibrosis induced by a constitutively active transforming growth factor-β-receptor I.ResultsTreatment with pharmacologically relevant and well-tolerated doses of GNF6231 inhibited the activation of Wnt signalling in fibrotic murine skin. GNF6231 ameliorated skin fibrosis in all four models. Treatment with GNF6231 also reduced pulmonary fibrosis associated with murine cGvHD. Most importantly, GNF6231 prevented progression of fibrosis and showed evidence of reversal of established fibrosis.ConclusionsThese data suggest that targeting the Wnt pathway through inhibition of porcupine provides a potential therapeutic approach to fibrosis in SSc. This is of particular interest, as a close analogue of GNF6231 has already demonstrated robust pathway inhibition in humans and could be available for clinical trials.

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37

OMATA, Masao. "Regression of Liver Fibrosis in Patients Treated By Interferon." Internal Medicine 43, no. 10 (2004): 887–88. http://dx.doi.org/10.2169/internalmedicine.43.887.

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38

Weber, Karl T., Yao Sun, Ivan C. Gerling, and Ramareddy V. Guntaka. "Regression of Established Cardiac Fibrosis in Hypertensive Heart Disease." American Journal of Hypertension 30, no. 11 (April 3, 2017): 1049–52. http://dx.doi.org/10.1093/ajh/hpx054.

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39

Bitsch, M., H. H. Nørgaard, O. Røder, T. V. Schroeder, and J. E. Lorentzen. "Inflammatory aortic aneurysms: Regression of fibrosis after aneurysm surgery." European Journal of Vascular and Endovascular Surgery 13, no. 4 (April 1997): 371–74. http://dx.doi.org/10.1016/s1078-5884(97)80078-0.

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40

Boffa, Jean-Jacques, Pierre-Louis Tharaux, Jean-Claude Dussaule, and Christos Chatziantoniou. "Regression of Renal Vascular Fibrosis by Endothelin Receptor Antagonism." Hypertension 37, no. 2 (February 2001): 490–96. http://dx.doi.org/10.1161/01.hyp.37.2.490.

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41

Habib, A., J. Wan, P. Hedge, E. Weiss, A. Brouillet, J. Lodder, R. Moreau, and S. Lotersztajn. "P0426 : Inhibition of monoacylglycerol lipase accelerates liver fibrosis regression." Journal of Hepatology 62 (April 2015): S472—S473. http://dx.doi.org/10.1016/s0168-8278(15)30636-x.

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42

Castera, Laurent. "Non-invasive tests for liver fibrosis progression and regression." Journal of Hepatology 64, no. 1 (January 2016): 232–33. http://dx.doi.org/10.1016/j.jhep.2015.10.011.

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Chatziantoniou, Christos, Jean-Jacques Boffa, Pierre-Louis Tharaux, Martin Flamant, Pierre Ronco, and Jean-Claude Dussaule. "Progression and regression in renal vascular and glomerular fibrosis." International Journal of Experimental Pathology 85, no. 1 (April 26, 2004): 1–11. http://dx.doi.org/10.1111/j.0959-9673.2004.00376.x.

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Kitamura, Haruki Kume, Tadaichi. "Spontaneous Regression of Bilateral Hydronephrosis due to Retroperitoneal Fibrosis." Scandinavian Journal of Urology and Nephrology 35, no. 3 (January 2001): 255–56. http://dx.doi.org/10.1080/003655901750292105.

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45

Baggs, R. B., J. Ferin, and G. Oberdörster. "Regression of Pulmonary Lesions Produced by Inhaled Titanium Dioxide in Rats." Veterinary Pathology 34, no. 6 (November 1997): 592–97. http://dx.doi.org/10.1177/030098589703400607.

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Inhaled ultrafine particles of TiO2 (TiO2-D, 20 nm particle size) lead to a greater pulmonary inflammatory response than larger pigment-grade particles (TiO2-F, 250 nm). Male Fisher 344 rats were exposed for 6 hours a day, 5 days a week, for 3 months to 1) filtered air (control); 2) TiO2-F, 22.3 mg/m3; 3) TiO2-D, 23.5 mg/m3; or 4) crystalline SiO2, a positive control particle (∼ 800 nm particle size, 1.3 mg/m3). Groups of 3-4 animals were sacrificed at 6 and 12 months following the completion of exposure. Pulmonary effects of exposure were evaluated using standard hematoxylin and eosin–stain sections, histochemical stains for collagen, and immunohistochemical assays for cell turnover. Six months after animals were exposed to SiO2, they had moderate focal interstitial fibrosis and moderately severe focal alveolitis. Animals exposed to TiO2-D had slightly less fibrosis. The least fibrosis was seen in the TiO2-F group. At 1 year after exposure, fibrosis was still present but decreased in the SiO2 group. The amount of interstitial fibrosis in the TiO2-D– and TiO2-F–treated animals had largely returned to untreated control levels, although an increased number of alveolar macrophages persisted, usually with retained particles. There was discordance between bromodeoxyuridine and proliferating cell nuclear antigen indices, most probably due to cytokine elaboration in the areas of inflammation, which may have altered the expression of proliferating cell nuclear antigens. There was no detectable fibroblast labeling at the 6-month observation and only very low levels at 12 months. Thus, although initially irritant, TiO2-induced lesions regressed during a 1-year period following cessation of exposure.

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Bozkurt, Devrim, Selahattin Bicak, Savas Sipahi, Huseyin Taskin, Ender Hur, Muhittin Ertilav, Sait Şen, and Soner Duman. "The Effects of Colchicine on the Progression and Regression of Encapsulating Peritoneal Sclerosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 5_suppl (September 2008): 53–57. http://dx.doi.org/10.1177/089686080802805s11.

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Background Encapsulating peritoneal sclerosis (EPS) is an infrequent but extremely serious complication of long-term peritoneal dialysis. Fibrosis of the submesothelial compact zone and neoangiogenesis underlie the pathophysiology of EPS. Colchicine is a well-known anti-inflammatory and antifibrotic agent that has been used for some fibrosing clinical states, such as liver fibrosis. Objective To determine the antifibrotic and anti-inflammatory effects of colchicine in an EPS rat model in both progression (P) and regression (R). Methods 48 nonuremic albino Wistar rats were divided into 5 groups: control group, 2 mL isotonic saline intraperitoneally (IP) daily for 3 weeks; CG group, IP injection of 2 mL/200 g chlorhexidine gluconate (CG) (0.1%) and ethanol (15%) dissolved in saline, daily for 3 weeks; resting group, CG (0 – 3 weeks) + peritoneal resting (4 – 6 weeks); C-R group, CG (0 – 3 weeks) + 1 mg/L colchicine (4 – 6 weeks); C-P group, CG (0 – 3 weeks) + 1 mg/L colchicine in drinking water (0 – 3 weeks). At the end, a 1-hour peritoneal equilibration test was performed with 25 mL 3.86% peritoneal dialysis solution. Dialysate-to-plasma ratio of urea (D/P urea), dialysate WBC count, ultrafiltration volume, and morphological changes of parietal peritoneum were examined. Result Exposure to CG for 3 weeks resulted in alterations in peritoneal transport (increased D/P urea, decreased ultrafiltration volume; p < 0.05) and morphology (increased inflammation, neovascularization, fibrosis, and peritoneal thickness; p < 0.05). Resting had some beneficial effects on peritoneal derangements; however, once the peritoneum had been stimulated, resting alone was not enough to reverse these pathological changes. Colchicine had more pronounced effects on membrane integrity via decreased inflammation, cell infiltration, and vascularity compared to the resting group. Conclusion We suggest that colchicine may have therapeutic value in the management of EPS.

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Jangra, Anshika, Ashish Kothari, Phulen Sarma, Bikash Medhi, Balram Ji Omar, and Karanvir Kaushal. "Recent Advancements in Antifibrotic Therapies for Regression of Liver Fibrosis." Cells 11, no. 9 (April 29, 2022): 1500. http://dx.doi.org/10.3390/cells11091500.

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Cirrhosis is a severe form of liver fibrosis that results in the irreversible replacement of liver tissue with scar tissue in the liver. Environmental toxicity, infections, metabolic causes, or other genetic factors including autoimmune hepatitis can lead to chronic liver injury and can result in inflammation and fibrosis. This activates myofibroblasts to secrete ECM proteins, resulting in the formation of fibrous scars on the liver. Fibrosis regression is possible through the removal of pathophysiological causes as well as the elimination of activated myofibroblasts, resulting in the reabsorption of the scar tissue. To date, a wide range of antifibrotic therapies has been tried and tested, with varying degrees of success. These therapies include the use of growth factors, cytokines, miRNAs, monoclonal antibodies, stem-cell-based approaches, and other approaches that target the ECM. The positive results of preclinical and clinical studies raise the prospect of a viable alternative to liver transplantation in the near future. The present review provides a synopsis of recent antifibrotic treatment modalities for the treatment of liver cirrhosis, as well as a brief summary of clinical trials that have been conducted to date.

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Abdu, Suzan Bakr. "A new perspective in liver fibrosis: Etiology removal does not cause regression of liver fibrosis." Journal of Histology and Histopathology 5, no. 1 (2018): 6. http://dx.doi.org/10.7243/2055-091x-5-6.

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Ponsoye, Matthieu, Camelia Frantz, Nadira Ruzehaji, Carole Nicco, Muriel Elhai, Barbara Ruiz, Anne Cauvet, et al. "Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis." Annals of the Rheumatic Diseases 75, no. 12 (February 24, 2016): 2142–49. http://dx.doi.org/10.1136/annrheumdis-2015-208213.

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Supriono, Supriono, Asri Nugraheni, Handono Kalim, and Mudjiwijono Handaru Eko. "The Effect of Curcumin on Regression of Liver Fibrosis through Decreased Expression of Transforming Growth Factor-β1 (TGF-β1)." Indonesian Biomedical Journal 11, no. 1 (April 30, 2019): 52–8. http://dx.doi.org/10.18585/inabj.v11i1.463.

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BACKGROUND: Transforming growth factor (TGF)-β1 has a pivotal role in liver fibrogenesis. Curcumin effectively prevent the progression of liver fibrosis through inhibition of TGF-β1/Sma and drosophila MAD (Smad) signaling pathway. However, the role of curcumin in the regression of liver fibrosis is still unknown. This study investigated the role of curcumin and TGF-β1 in liver fibrosis regression.METHODS: An experimental Wistar rat model included 6 treatment groups as well as positive and negative control groups. The treatment and positive control groups were injected with carbon tetrachlorid (CCl4) for 9 weeks to induce liver fibrosis. After cessation of injection, 3 of the treatment groups were given curcumin and 3 were given carboxymethylcellulose (CMC) for 2, 5 and 9 weeks, while the positive control was untreated. The negative control was injected with normal saline. TGF-β1 liver tissue levels were analyzed by ELISA, while the TGF-β1 expression in liver cells was analyzed by immunohistochemical assay. The metavir score was used to assess the degree of liver fibrosis. Values of p<0.05 were regarded as statistically significant.RESULTS: Nine weeks of CCl4 injection induced liver fibrosis (metavir F3); and significantly increased TGF-β1 levels and expression in tissues (p=0.00, p=0.021, respectively). Curcumin administration decreased levels and expression of TGF-β1 in the liver and accelerated regression of liver fibrosis. There was a significant correlation between duration of administration of curcumin with an expression of TGF-β1 in the liver tissue (r=0.87; p<0.00).CONCLUSION: Curcumin accelerates regression of liver fibrosis, likely through decreasing of TGF-β1 expression in the liver.KEYWORDS: curcumin, TGF-β1, liver fibrosis regression, CCl4, animal model

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