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Статті в журналах з теми "Radiation-induced fibrosi"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Borrelli, Mimi R., Abra H. Shen, Gordon K. Lee, Arash Momeni, Michael T. Longaker, and Derrick C. Wan. "Radiation-Induced Skin Fibrosis." Annals of Plastic Surgery 83 (October 2019): S59—S64. http://dx.doi.org/10.1097/sap.0000000000002098.

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2

Kim, Jin-Mo, Hyun Yoo, Jee-Youn Kim, Sang Ho Oh, Jeong Wook Kang, Byung Rok Yoo, Song Yee Han, et al. "Metformin Alleviates Radiation-Induced Skin Fibrosis via the Downregulation of FOXO3." Cellular Physiology and Biochemistry 48, no. 3 (2018): 959–70. http://dx.doi.org/10.1159/000491964.

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Background/Aims: Radiation-induced skin fibrosis is a common side effect of clinical radiotherapy. Our previous next-generation sequencing (NGS) study demonstrated the reduced expression of the regulatory α subunit of phosphatidylinositol 3-kinase (PIK3r1) in irradiated murine skin. Metformin has been reported to target the PIK3-FOXO3 pathway. In this study, we investigated the effects of metformin on radiation-induced skin fibrosis. Methods: Metformin was orally administered to irradiated mice. Skin fibrosis was analyzed by staining with H&E and Masson’s trichrome stain. The levels of cytokines and chemokines associated with fibrosis were analyzed by immunohistochemistry and quantitative RT-PCR. The roles of PIK3rl and FOXO3 in radiation-induced skin fibrosis were studied by overexpressing PIK3rl and transfecting FOXO3 siRNA in NIH3T3 cells and mouse-derived dermal fibroblasts (MDF). Results: The oral administration of metformin significantly reduced radiation-induced skin thickening and collagen accumulation and significantly reduced the radiation-induced expression of FOXO3 in murine skin. Additionally, the overexpression of PIK3r1 reduced the radiation-induced expression of FOXO3, while FOXO3 silencing decreased the radiation-induced expression of TGFβ in vitro. Conclusions: The results indicated that metformin suppresses radiation-induced skin injuries by modulating the expression of FOXO3 through PIK3r1. Collectively, the data obtained in this study suggested that metformin could be a potent therapeutic agent for alleviating radiation-induced skin fibrosis.

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3

Topuzov, E. E., T. T. Agishev, K. A. Fedorov, D. A. Krasnozhon, A. B. Vats, D. V. Romanovsky, G. A. Dashyan, et al. "Transcutaneous oxegen measurement in the area of soft tissue radiation-induced fibrosis in patients with breast cancer." HERALD of North-Western State Medical University named after I.I. Mechnikov 10, no. 2 (December 15, 2018): 58–63. http://dx.doi.org/10.17816/mechnikov201810258-63.

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Late radiation injury in the form of radiation-induced fibrosis is one of the many complications of radiation therapy.In current literature, pathogenesis of radiation-induced fibrosis is considered from several angles. According to one of the hypotheses, the main cause of pathogenesis of radiation-induced fibrosis is damage of the blood vessels caused by radiation. Another hypothesis insists that radiation causes depletion of specific cell populations in the irradiated area, reducing the number of stem cells (mostly, fibroblasts). (For citation: Topuzov EE, Agishev TT, Fedorov КА, et al. Transcutaneous oxegen measurement in the area of soft tissue radiation-induced fibrosis in patients with breast cancer. Herald of North-Western State Medical University named after I.I. Mechnikov. 2018;10(2):58-63. doi: 10.17816/mechnikov201810258-63).

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4

Weigel, C., P. Schmezer, C. Plass, and O. Popanda. "Epigenetics in radiation-induced fibrosis." Oncogene 34, no. 17 (June 9, 2014): 2145–55. http://dx.doi.org/10.1038/onc.2014.145.

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5

Xavier, Sandhya, Ester Piek, Makiko Fujii, Delphine Javelaud, Alain Mauviel, Kathy C. Flanders, Ayelet M. Samuni, et al. "Amelioration of Radiation-induced Fibrosis." Journal of Biological Chemistry 279, no. 15 (January 19, 2004): 15167–76. http://dx.doi.org/10.1074/jbc.m309798200.

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6

Hoeller, Ulrike, Michael Bonacker, Amira Bajrovic, Winfried Alberti, and Gustav Adam. "Radiation-Induced Plexopathy and Fibrosis." Strahlentherapie und Onkologie 180, no. 10 (October 2004): 650–54. http://dx.doi.org/10.1007/s00066-004-1240-3.

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7

Blakaj, A., X. Chi, W. F. Mourad, E. Herzog, L. Leng, and R. Bucala. "Metallothioneins in Fibrosis: Implications for Radiation-Induced Fibrosis." International Journal of Radiation Oncology*Biology*Physics 90, no. 1 (September 2014): S684—S685. http://dx.doi.org/10.1016/j.ijrobp.2014.05.2011.

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8

Liu, Chun-Shan, Reka Toth, Ali Bakr, Ashish Goyal, Md Saiful Islam, Kersten Breuer, Anand Mayakonda, et al. "Epigenetic Modulation of Radiation-Induced Diacylglycerol Kinase Alpha Expression Prevents Pro-Fibrotic Fibroblast Response." Cancers 13, no. 10 (May 18, 2021): 2455. http://dx.doi.org/10.3390/cancers13102455.

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Radiotherapy, a common component in cancer treatment, can induce adverse effects including fibrosis in co-irradiated tissues. We previously showed that differential DNA methylation at an enhancer of diacylglycerol kinase alpha (DGKA) in normal dermal fibroblasts is associated with radiation-induced fibrosis. After irradiation, the transcription factor EGR1 is induced and binds to the hypomethylated enhancer, leading to increased DGKA and pro-fibrotic marker expression. We now modulated this DGKA induction by targeted epigenomic and genomic editing of the DGKA enhancer and administering epigenetic drugs. Targeted DNA demethylation of the DGKA enhancer in HEK293T cells resulted in enrichment of enhancer-related histone activation marks and radiation-induced DGKA expression. Mutations of the EGR1-binding motifs decreased radiation-induced DGKA expression in BJ fibroblasts and caused dysregulation of multiple fibrosis-related pathways. EZH2 inhibitors (GSK126, EPZ6438) did not change radiation-induced DGKA increase. Bromodomain inhibitors (CBP30, JQ1) suppressed radiation-induced DGKA and pro-fibrotic marker expression. Similar drug effects were observed in donor-derived fibroblasts with low DNA methylation. Overall, epigenomic manipulation of DGKA expression may offer novel options for a personalized treatment to prevent or attenuate radiotherapy-induced fibrosis.

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9

Horton, Jason A., Fei Li, Eun Joo Chung, Kathryn Hudak, Ayla White, Kristopher Krausz, Frank Gonzalez, and Deborah Citrin. "Quercetin Inhibits Radiation-Induced Skin Fibrosis." Radiation Research 180, no. 2 (July 2, 2013): 205. http://dx.doi.org/10.1667/rr3237.1.

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10

Rosenbloom, Joel. "Therapeutic Approaches to Radiation-Induced Fibrosis." Journal of Cancer Treatment and Diagnosis 2, no. 4 (August 1, 2018): 7–9. http://dx.doi.org/10.29245/2578-2967/2018/4.1144.

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11

&NA;. "Tamoxifen increases radiation-induced lung fibrosis." Reactions Weekly &NA;, no. 617 (September 1996): 4. http://dx.doi.org/10.2165/00128415-199606170-00008.

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12

Rodemann, H. Peter, and Michael Bamberg. "Cellular basis of radiation-induced fibrosis." Radiotherapy and Oncology 35, no. 2 (May 1995): 83–90. http://dx.doi.org/10.1016/0167-8140(95)01540-w.

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13

Yang, Shanmin, Mei Zhang, Chun Chen, Yongbin Cao, Yeping Tian, Yangsong Guo, Bingrong Zhang, et al. "Triptolide Mitigates Radiation-Induced Pulmonary Fibrosis." Radiation Research 184, no. 5 (October 21, 2015): 509. http://dx.doi.org/10.1667/rr13831.1.

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14

LEE, Y. C., A. E. TRIBE, and A. W. MUSK. "Chylothorax from radiation-induced mediastinal fibrosis." Australian and New Zealand Journal of Medicine 28, no. 5 (October 1998): 667–68. http://dx.doi.org/10.1111/j.1445-5994.1998.tb00670.x.

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15

Kumar, R., M. Griffin, G. Adigbli, N. Kalavrezos, and P. E. M. Butler. "Lipotransfer for radiation-induced skin fibrosis." British Journal of Surgery 103, no. 8 (May 12, 2016): 950–61. http://dx.doi.org/10.1002/bjs.10180.

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16

Yahyapour, Rasoul, Peyman Amini, Hana Saffar, Elahe Motevaseli, Bagher Farhood, Vahid Pooladvand, Dheyauldeen Shabeeb, Ahmed Eleojo Musa, and Masoud Najafi. "Protective Effect of Metformin, Resveratrol and Alpha-lipoic Acid on Radiation- Induced Pneumonitis and Fibrosis: A Histopathological Study." Current Drug Research Reviews 11, no. 2 (December 10, 2019): 111–17. http://dx.doi.org/10.2174/2589977511666191018180758.

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Background: Radiation-induced pneumonitis and fibrosis are the most common side effects of chest radiotherapy. They result from massive and chronic production of Reactive Oxygen Species (ROS), inhibition of antioxidant enzymes as well as the release of several inflammatory mediators. In this study, we aimed to detect the radioprotective effects of metformin (as inhibitor of mitochondrial ROS), resveratrol (as stimulator of antioxidant defense enzymes) and alpha-lipoic acid (as direct antioxidant) for alleviating radiation-induced pneumonitis and fibrosis. Methods: 80 Male Mice were randomly allotted to eight groups which include G1: control; G2: resveratrol; G3: alpha-lipoic acid; G4: metformin; G5: radiation; G6: radiation plus resveratrol; G7: radiation plus alpha-lipoic acid; G8: radiation plus metformin. Drugs’ doses were as follows: 100 mg/kg metformin, 200 mg/kg resveratrol and 200 mg/kg alpha-lipoic acid. Irradiation with a single radiation dose of 18 Gy was performed using a cobalt-60 (60Co) gamma-ray source. After 80 days, all mice were sacrificed and their lung tissues evaluated for morphological changes using histopathological markers. Results: Irradiation led to acute pneumonitis including infiltration of inflammatory cells and damages to alveolar and vascular, as well as mild fibrosis. Metformin, alpha-lipoic acid and resveratrol were able to reduce pneumonitis and overcome radiation-induced fibrosis. Conclusion: All agents could protect against radiation-induced lung injury moderately. It is possible that administering higher doses of these drugs over a long period of time could give better radioprotection of the lung.

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17

Judge, J. L., K. M. Owens, S. J. Pollock, C. F. Woeller, T. H. Thatcher, J. P. Williams, R. P. Phipps, P. J. Sime, and R. M. Kottmann. "Ionizing radiation induces myofibroblast differentiation via lactate dehydrogenase." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 8 (October 15, 2015): L879—L887. http://dx.doi.org/10.1152/ajplung.00153.2015.

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Pulmonary fibrosis is a common and dose-limiting side-effect of ionizing radiation used to treat cancers of the thoracic region. Few effective therapies are available for this disease. Pulmonary fibrosis is characterized by an accumulation of myofibroblasts and excess deposition of extracellular matrix proteins. Although prior studies have reported that ionizing radiation induces fibroblast to myofibroblast differentiation and collagen production, the mechanism remains unclear. Transforming growth factor-β (TGF-β) is a key profibrotic cytokine that drives myofibroblast differentiation and extracellular matrix production. However, its activation and precise role in radiation-induced fibrosis are poorly understood. Recently, we reported that lactate activates latent TGF-β through a pH-dependent mechanism. Here, we wanted to test the hypothesis that ionizing radiation leads to excessive lactate production via expression of the enzyme lactate dehydrogenase-A (LDHA) to promote myofibroblast differentiation. We found that LDHA expression is increased in human and animal lung tissue exposed to ionizing radiation. We demonstrate that ionizing radiation induces LDHA, lactate production, and extracellular acidification in primary human lung fibroblasts in a dose-dependent manner. We also demonstrate that genetic and pharmacologic inhibition of LDHA protects against radiation-induced myofibroblast differentiation. Furthermore, LDHA inhibition protects from radiation-induced activation of TGF-β. We propose a profibrotic feed forward loop, in which radiation induces LDHA expression and lactate production, which can lead to further activation of TGF-β to drive the fibrotic process. These studies support the concept of LDHA as an important therapeutic target in radiation-induced pulmonary fibrosis.

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18

Ma, Chengxu, Xinke Zhao, Juan Chang, Huan Guo, Huiping Wei, Zhaoyuan Fu, and Yingdong Li. "Radix Angelica Sinensis and Radix Hedysari Ultrafiltration Extract Protects against X-Irradiation-Induced Cardiac Fibrosis in Rats." Evidence-Based Complementary and Alternative Medicine 2020 (April 21, 2020): 1–9. http://dx.doi.org/10.1155/2020/4675851.

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Radiation-induced myocardial fibrosis (RIMF) is the main pathological change associated with radiation-induced heart toxicity after radiation therapy in patients with thoracic tumors. There is an antifibrosis effect of Radix Angelica Sinensis and Radix Hedysari (RAS-RH) ultrafiltration extract from Danggui Buxue decoction (DBD) in X-irradiation-induced rat myocardial fibrosis, and this study aimed to investigate whether that effect correlated with apoptosis and oxidative stress damage in primary rat cardiac fibroblasts; further, the potential mechanisms were also explored. In this study, we first found that the RAS-RH antifibrosis effect was associated with the upregulation of microRNA-200a and the downregulation of TGF-β1/smad3 and COL1α. In addition, we also found that the antifibrosis effect of RAS-RH was related to the induction of apoptosis in primary rat cardiac fibroblasts and to the prevention of damage caused by reactive oxygen species (ROS). Interestingly, primary rat cardiac fibroblasts exposed to X-ray radiation underwent apoptosis less frequently in the absence of RAS-RH. Therefore, RAS-RH has the ability to protect against fibrosis, which could be occurring through the induction of apoptosis and the resistance to oxidative stress in rats with X-irradiation-induced myocardial fibrosis; thus, in a model of RIMF, RAS-RH acts against X-irradiation-induced cardiac toxicity.

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19

Zanoni, Cortesi, Zamagni, and Tesei. "The Role of Mesenchymal Stem Cells in Radiation-Induced Lung Fibrosis." International Journal of Molecular Sciences 20, no. 16 (August 8, 2019): 3876. http://dx.doi.org/10.3390/ijms20163876.

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Radiation therapy is one of the most important treatment modalities for thoracic tumors. Despite significant advances in radiation techniques, radiation-induced lung injury (RILI) still occurs in up to 30% of patients undergoing thoracic radiotherapy, and therefore remains the main dose-limiting obstacle. RILI is a potentially lethal clinical complication of radiotherapy that has 2 main stages: an acute stage defined as radiation pneumonitis, and a late stage defined as radiation-induced lung fibrosis. Patients who develop lung fibrosis have a reduced quality of life with progressive and irreversible organ malfunction. Currently, the most effective intervention for the treatment of lung fibrosis is lung transplantation, but the lack of available lungs and transplantation-related complications severely limits the success of this procedure. Over the last few decades, advances have been reported in the use of mesenchymal stem cells (MSCs) for lung tissue repair and regeneration. MSCs not only replace damaged lung epithelial cells but also promote tissue repair through the secretion of anti-inflammatory and anti-fibrotic factors. Here, we present an overview of MSC-based therapy for radiation-induced lung fibrosis, focusing in particular on the molecular mechanisms involved and describing the most recent preclinical and clinical studies carried out in the field.

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20

Wang, Lu-Kai, Tsai-Jung Wu, Ji-Hong Hong, Fang-Hsin Chen, John Yu, Chun-Chieh Wang, and Andrea Ballini. "Radiation Induces Pulmonary Fibrosis by Promoting the Fibrogenic Differentiation of Alveolar Stem Cells." Stem Cells International 2020 (September 29, 2020): 1–12. http://dx.doi.org/10.1155/2020/6312053.

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The lung is a radiosensitive organ, which imposes limits on the therapeutic dose in thoracic radiotherapy. Irradiated alveolar epithelial cells promote radiation-related pneumonitis and fibrosis. However, the role of lung stem cells (LSCs) in the development of radiation-induced lung injury is still unclear. In this study, we found that both LSCs and LSC-derived type II alveolar epithelial cells (AECII) can repair radiation-induced DNA double-strand breaks, but the irradiated LSCs underwent growth arrest and cell differentiation faster than the irradiated AECII cells. Moreover, radiation drove LSCs to fibrosis as shown with the elevated levels of markers for epithelial-mesenchymal transition and myofibroblast (α-smooth muscle actin (α-SMA)) differentiation in in vitro and ex vivo studies. Increased gene expressions of connective tissue growth factor and α-SMA were found in both irradiated LSCs and alveolar cells, suggesting that radiation could induce the fibrogenic differentiation of LSCs. Irradiated LSCs showed an increase in the expression of surfactant protein C (SP-C), the AECII cell marker, and α-SMA, and irradiated AECII cells expressed SP-C and α-SMA. These results indicated that radiation induced LSCs to differentiate into myofibroblasts and AECII cells; then, AECII cells differentiated further into either myofibroblasts or type I alveolar epithelial cells (AECI). In conclusion, our results revealed that LSCs are sensitive to radiation-induced cell damage and may be involved in radiation-induced lung fibrosis.

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21

Zhu, Yanfei, Jing Zhou, and Guoqing Tao. "Molecular aspects of chronic radiation enteritis." Clinical & Investigative Medicine 34, no. 3 (June 1, 2011): 119. http://dx.doi.org/10.25011/cim.v34i3.15183.

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Purpose: Chronic radiation enteritis (CRE) is one of the most feared complications of abdominal or pelvic radiation therapy and the treatment of CRE is difficult and often controversial. Recent progress in molecular biology has shed some light on the pathogenesis of CRE, which is characterized by fibrosis. The purpose of this article is to summarize the current state of knowledge of molecular aspects of radiation induced intestinal fibrosis and to discuss potential therapeutic targets. Methods: A review of the up-to-date published literature involving the possible molecular cascades in radiation-induced intestinal fibrosis and prospective targets for CRE were performed using the Pub-Med search engine. Results: Fibrosis development is correlated with transforming growth factor β1 (TGF-β1) and its downstream effector Smad3, which stimulates ﬁbrogenic downstream mediators, such as connective tissue growth factor (CTGF). Ras homologue (Rho) and Rho-associated kinase (ROCK) signaling pathway have been shown to play important roles in the development of CRE. The inhibition of these pathways ameliorated radiation-induced intestinal fibrosis in vitro and in animal studies; however, the relationship between the Smad3 and Rho signaling pathways has not been elucidated. Conclusions: Rho/ROCK and TGF-β1/Smad3 signaling pathways have been shown to play a key role in intestinal fibrogenesis, which might provide with effective possibilities for clinical intervention. Understanding the cooperation between Smad3 and Rho, may therefore be critical to our overall understanding of fibrosis development and maintenance of CRE.

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22

Jin, Hee, Youngjo Yoo, Younghwa Kim, Yeijin Kim, Jaeho Cho, and Yun-Sil Lee. "Radiation-Induced Lung Fibrosis: Preclinical Animal Models and Therapeutic Strategies." Cancers 12, no. 6 (June 12, 2020): 1561. http://dx.doi.org/10.3390/cancers12061561.

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Radiation-induced lung injury (RILI), including acute radiation pneumonitis and chronic radiation-induced lung fibrosis, is the most common side effect of radiation therapy. RILI is a complicated process that causes the accumulation, proliferation, and differentiation of fibroblasts and, finally, results in excessive extracellular matrix deposition. Currently, there are no approved treatment options for patients with radiation-induced pulmonary fibrosis (RIPF) partly due to the absence of effective targets. Current research advances include the development of small animal models reflecting modern radiotherapy, an understanding of the molecular basis of RIPF, and the identification of candidate drugs for prevention and treatment. Insights provided by this research have resulted in increased interest in disease progression and prognosis, the development of novel anti-fibrotic agents, and a more targeted approach to the treatment of RIPF.

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23

Liang, Jianye, Xiubao Song, Zeyu Xiao, Hanwei Chen, Changzheng Shi, and Liangping Luo. "Using IVIM-MRI and R2⁎ Mapping to Differentiate Early Stage Liver Fibrosis in a Rat Model of Radiation-Induced Liver Fibrosis." BioMed Research International 2018 (December 3, 2018): 1–9. http://dx.doi.org/10.1155/2018/4673814.

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Rationale and Objectives. To investigate the utility of intravoxel incoherent motion MRI (IVIM-MRI) and R2⁎ mapping in diagnosing early stage liver fibrosis in a radiation-induced rat model. Materials and Methods. Thirty rats were randomly divided into three groups with 10 rats in each group. Liver fibrosis was induced by exposure of right lobe of liver in each animal to 20 Gy of radiation. MRI examination was conducted at baseline, one month, two months, and three months after radiation using T1WI, T2WI, IVIM-DWI, and R2⁎ sequences. The pathological examination included hematoxylin eosin, masson trichrome, and prussian blue staining. D, D⁎, f, and R2⁎ values were measured in both left and right lobes for quantitative analysis. Results. Regarding the surviving 23 rats, eight rats were diagnosed with stage F0, ten with stage F1, and five with stage F2 liver fibrosis using METAVIR Scores. The D values of right lobes decreased (P<0.05), and R2⁎ values increased (P<0.01) significantly as fibrosis levels increased. But there was no statistical difference in D⁎ (P=0.970) and f values (P=0.079). R2⁎ value showed a strong positive correlation (r=0.819, P<0.001), while D value showed a negative correlation with fibrosis stages (r=-0.424, P<0.001). D⁎ (r=0.029, P=0.744) and f values (r=-0.055, P=0.536) were poorly correlated with fibrosis levels. Conclusion. IVIM-MRI and R2⁎ mapping are useful techniques for evaluating the severity of liver fibrosis in a radiation-induced rat model, and R2⁎ value is the most sensitive parameter in detecting early stage fibrosis.

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24

Gervaz, Pascal, Philippe Morel, and Marie-Catherine Vozenin-Brotons. "Molecular Aspects of Intestinal Radiation-Induced Fibrosis." Current Molecular Medicine 9, no. 3 (April 1, 2009): 273–80. http://dx.doi.org/10.2174/156652409787847164.

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25

Bese, N. S., A. Y. Altinok, E. M. Ozsahin, S. Yildirim, N. Sut, T. Altug, A. Ober, and D. Azria. "Aromatase inhibitors and radiation-induced lung fibrosis." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 614. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.614.

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26

He, Yonghan, Dinesh Thummuri, Guangrong Zheng, Paul Okunieff, Deborah E. Citrin, Zeljko Vujaskovic, and Daohong Zhou. "Cellular senescence and radiation-induced pulmonary fibrosis." Translational Research 209 (July 2019): 14–21. http://dx.doi.org/10.1016/j.trsl.2019.03.006.

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27

Rodemann, H. P. "294The cellular basis of radiation-induced fibrosis." Radiotherapy and Oncology 40 (January 1996): S77. http://dx.doi.org/10.1016/s0167-8140(96)80303-3.

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28

Soule, B. P., C. B. Simone, A. Sowers, J. B. Mitchell, and N. L. Simone. "TH2 Cytokines Mediate Late Radiation-induced Fibrosis." Journal of Allergy and Clinical Immunology 125, no. 2 (February 2010): AB110. http://dx.doi.org/10.1016/j.jaci.2009.12.433.

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29

Huitink, Johannes M., and Lambert Zijp. "Laryngeal Radiation Fibrosis: A Case of Failed Awake Flexible Fibreoptic Intubation." Case Reports in Anesthesiology 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/878910.

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Awake fibreoptic intubation is accepted as the gold standard for intubation of patients with an anticipated difficult airway. Radiation fibrosis may cause difficulties during the intubation procedure. We present an unusual severe case of radiation induced changes to the larynx, with limited clinical symptoms, that caused failure of the fibreoptic intubation technique. A review of the known literature on radiation fibrosis and airway management is presented.

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30

Meng, Guanmin, Melinda Wuest, Xiaoyun Tang, Jennifer Dufour, Todd P. W. McMullen, Frank Wuest, David Murray, and David N. Brindley. "Dexamethasone Attenuates X-Ray-Induced Activation of the Autotaxin-Lysophosphatidate-Inflammatory Cycle in Breast Tissue and Subsequent Breast Fibrosis." Cancers 12, no. 4 (April 18, 2020): 999. http://dx.doi.org/10.3390/cancers12040999.

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We recently showed that radiation-induced DNA damage in breast adipose tissue increases autotaxin secretion, production of lysophosphatidate (LPA) and expression of LPA1/2 receptors. We also established that dexamethasone decreases autotaxin production and LPA signaling in non-irradiated adipose tissue. In the present study, we showed that dexamethasone attenuated the radiation-induced increases in autotaxin activity and the concentrations of inflammatory mediators in cultured human adipose tissue. We also exposed a breast fat pad in mice to three daily 7.5 Gy fractions of X-rays. Dexamethasone attenuated radiation-induced increases in autotaxin activity in plasma and mammary adipose tissue and LPA1 receptor levels in adipose tissue after 48 h. DEX treatment during five daily fractions of 7.5 Gy attenuated fibrosis by ~70% in the mammary fat pad and underlying lungs at 7 weeks after radiotherapy. This was accompanied by decreases in CXCL2, active TGF-β1, CTGF and Nrf2 at 7 weeks in adipose tissue of dexamethasone-treated mice. Autotaxin was located at the sites of fibrosis in breast tissue and in the underlying lungs. Consequently, our work supports the premise that increased autotaxin production and lysophosphatidate signaling contribute to radiotherapy-induced breast fibrosis and that dexamethasone attenuated the development of fibrosis in part by blocking this process.

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Ma, Cheng-Xu, Xin-Ke Zhao, and Ying-Dong Li. "New therapeutic insights into radiation-induced myocardial fibrosis." Therapeutic Advances in Chronic Disease 10 (January 2019): 204062231986838. http://dx.doi.org/10.1177/2040622319868383.

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Radiation therapy (RT) for the treatment of thoracic tumors causes radiation-induced heart disease (RIHD). Radiation-induced myocardial fibrosis (RIMF) is both an acute and chronic stage of RIHD, depending on the specific pathology, and is thought to be a major risk factor for adverse myocardial remodeling and vascular changes. With the use of more three-dimensional conformal radiation regimens and early screenings and diagnoses for RIMF, the incidence of RIHD is declining, but it still must be carefully investigated to minimize the mortality and morbidity of patients with thoracic malignancies after RT treatment. Effective methods for preventing RIMF involve a decrease in the direct radiation dose in the heart, and early screening and diagnosis. Medications remain as a useful adjunct for preventing or treating RIMF. This review mainly discusses the cellular and molecular mechanisms underlying RIMF, and new therapeutic drugs that can potentially be developed from this knowledge.

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Rødningen, Olaug Kristin, Anne-Lise Børresen-Dale, Jan Alsner, Trevor Hastie, and Jens Overgaard. "Radiation-induced gene expression in human subcutaneous fibroblasts is predictive of radiation-induced fibrosis." Radiotherapy and Oncology 86, no. 3 (March 2008): 314–20. http://dx.doi.org/10.1016/j.radonc.2007.09.013.

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Shrishrimal, Shashank, Elizabeth A. Kosmacek, and Rebecca E. Oberley-Deegan. "Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis." Oxidative Medicine and Cellular Longevity 2019 (February 6, 2019): 1–27. http://dx.doi.org/10.1155/2019/4278658.

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Radiation-induced fibrosis (RIF) develops months to years after initial radiation exposure. RIF occurs when normal fibroblasts differentiate into myofibroblasts and lay down aberrant amounts of extracellular matrix proteins. One of the main drivers for developing RIF is reactive oxygen species (ROS) generated immediately after radiation exposure. Generation of ROS is known to induce epigenetic changes and cause differentiation of fibroblasts to myofibroblasts. Several antioxidant compounds have been shown to prevent radiation-induced epigenetic changes and the development of RIF. Therefore, reviewing the ROS-linked epigenetic changes in irradiated fibroblast cells is essential to understand the development and prevention of RIF.

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Escott, C., N. A. Madden, E. Schreibmann, S. Tian, R. J. Cassidy, A. I. Sutter, D. Whitaker, et al. "Radiomic Analysis of Radiation Induced Fibrosis Following Stereotactic Body Radiation Therapy." International Journal of Radiation Oncology*Biology*Physics 105, no. 1 (September 2019): E505—E506. http://dx.doi.org/10.1016/j.ijrobp.2019.06.1327.

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Kunwar, Amit, and Christina K. Haston. "Basal levels of glutathione peroxidase correlate with onset of radiation induced lung disease in inbred mouse strains." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 8 (October 15, 2014): L597—L604. http://dx.doi.org/10.1152/ajplung.00088.2014.

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Biomarkers predicting for the radiation-induced lung responses of pneumonitis or fibrosis are largely unknown. Herein we investigated whether markers of oxidative stress and intracellular antioxidants, measured within days of radiation exposure, are correlated with the lung tissue injury response occurring weeks later. Mice of the eight inbred strains differing in their susceptibility to radiation-induced pulmonary fibrosis, and in the duration of asymptomatic survival, received 18 Gy whole thorax irradiation and were killed 6 h, 24 h, or 7 days later. Control mice were not irradiated. Lung levels of antioxidants superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione, and of oxidative damage [reactive oxygen species (ROS) and 8-hydroxydeoxyguanosine (8-OHdG)], were biochemically determined. GPx was additionally measured through gene expression and immunohistochemical assessment of lung tissue, and activity in serum. ROS and 8-OHdG were increased postirradiation and exhibited significant strain and time-dependent variability, but were not strongly predictive of radiation-induced lung diseases. Antioxidant measures were not dramatically changed postirradiation and varied significantly among the strains. Basal GPx activity ( r = 0.73, P = 0.04) in the lung and the pulmonary expression of GPx2 ( r = 0.94, P = 0.0003) correlated with postirradiation asymptomatic survival, whereas serum GPx activity was inversely correlated ( r = −0.80, P = 0.01) with fibrosis development. In conclusion, pulmonary oxidative stress and antioxidant markers were more affected by inbred strain than radiation over 7 days posttreatment. Lung GPx activity, and GPx2 expression, predicted for survival from lethal pneumonitis, and serum GPx for fibrosis, in this panel of mice.

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Horton, Jason A., Eun Joo Chung, Kathryn E. Hudak, Anastasia Sowers, Angela Thetford, Ayla O. White, James B. Mitchell, and Deborah E. Citrin. "Inhibition of radiation-induced skin fibrosis with imatinib." International Journal of Radiation Biology 89, no. 3 (November 19, 2012): 162–70. http://dx.doi.org/10.3109/09553002.2013.741281.

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Okunieff, Paul, Elizabeth Augustine, Jeanne E. Hicks, Terri L. Cornelison, Rosemary M. Altemus, Boris G. Naydich, Ivan Ding, et al. "Pentoxifylline in the Treatment of Radiation-Induced Fibrosis." Journal of Clinical Oncology 22, no. 11 (June 1, 2004): 2207–13. http://dx.doi.org/10.1200/jco.2004.09.101.

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Purpose Fibrotic sequelae remain the most important dose-limiting toxicity of radiation therapy to soft tissue. Functionally, this is reflected in loss of range of motion and muscle strength and the development of limb edema and pain. Tumor necrosis factor alpha and fibroblast growth factor 2 (FGF2), which are abnormally elevated in irradiated tissues, may mediate radiation fibrovascular injury. Patients and Methods In an open label drug trial, we studied the effects of pentoxifylline (400 mg orally tid for 8 weeks) on 30 patients who displayed late, radiation-induced fibrosis at 1 to 29 years posttreatment (40 to 84 Gy). The primary outcome measurement was change in physical impairments thought to be secondary to radiation, including active and passive range of motion (AROM and PROM), muscle strength, limb edema, and pain. Plasma levels of cytokines (tumor necrosis factor alpha and FGF2) also were measured. Twenty-seven patients completed baseline and 8-week assessments, and 24 patients completed baseline, 8-week, and 16-week assessments. Results After 8 weeks of pentoxifylline intervention, 20 of 23 patients with impaired AROM and 19 of 22 with impaired PROM improved; 11 of 19 patients with muscle weakness showed improved motor strength; five of seven patients with edema had decreased limb girth; and nine of 20 patients had decreased pain. Pretreatment FGF2 levels dropped from an average of 44.9 pg/mL to 24.0 pg/mL after 8 weeks of treatment. Conclusion Patients receiving pentoxifylline demonstrated improved AROM, PROM, and muscle strength and decreased limb edema and pain. Reversal of these delayed radiation effects was associated with a decrease in circulating FGF2.

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Maklad, Ahmed M., Hanan Abdel-Rady Assaf, Essameldin Abdelaziz Nada, Ashraf Elyamany, and Asmaa A. Badran. "Prognostic factors affecting severity of radiation-induced fibrosis." Journal of Clinical Oncology 34, no. 3_suppl (January 20, 2016): e280-e280. http://dx.doi.org/10.1200/jco.2016.34.3_suppl.e280.

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e280 Background: Evaluation of prognostic factors affecting Radiation Induced Fibrosis (RIF) to help for decreasing its incidence and to improve quality of life for cancer survivors. Methods: Thirty patients were included in this study .It was carried out at faculty of medicine, Sohag University Hospital, Egypt during the period between July 2012 and July 2013 after approval of university ethical committee. We included all patients with (RIF) which is persistent or appeared after 6 months of completion of radiation therapy. Detailed medical history and clinical examination were done for all patients included in the study. We categorized the patients according to severity of RIF into four grades according RTO 2010. Assessment of pain was done according to 0–10 Numeric Pain Rating Scale. Results: Thirty patients with RIF were included in the study. The age of the studied patients ranged from 21- 65 years with a Mean 48,33 ± SD of 10,88. 56.7% of the cases were more than 50 years old. Female patients were 73.3%. BMI of the studied patients ranged from 19-40 kg/cm2 with a Mean 28.03 ± SD of 6.98. 26.7%patients were smokers.43.3% patientshadprevious history of acute radio dermatitis.60% had breast tumor. Chest was affected in 19 (60%) patients, back in 3 (10%) patients, neck in 4 (13%) patients, lower limbs in 2 (7%) patients, and face in 2 (7%) patients.T1 represented in 30%, T2 in 36.7%, T3 in 13.3% while T4 in 20% of the included patients. Twenty four (80%) patientsreceived chemotherapy before radiation. We documented a significant relation between BMI and severity of RIF (p = 0.007).Severity of RIF was significantly associated with higher BMI (p = 0.007), higher radiation doses (p = 0.02), higher number of radiotherapy treatment fraction (p = 0.03), higher radiation field sizes (p = 0.003), and patients with duration of more than one year of RIF (p < 0.001). Patients from rural areas documented higher degree of RIF (p = 0.03). Conclusions: It is important to give more attention to RIF as a one of late toxicity of radiation therapy. It can be minimized by avoiding its predisposing factors to improve quality of life of cancer survivors.

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Wegrowski, J., J. L. Lefaix, and C. Lafuma. "Accumulation of Glycosaminoglycans in Radiation-induced Muscular Fibrosis." International Journal of Radiation Biology 61, no. 5 (January 1992): 685–93. http://dx.doi.org/10.1080/09553009214551501.

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Glatstein, E. "Pentoxifylline in the Treatment of Radiation-Induced Fibrosis." Yearbook of Oncology 2006 (January 2006): 27–28. http://dx.doi.org/10.1016/s1040-1741(08)70023-x.

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Calik, M., G. Yavas, E. Celik, C. Yavas, G. Calik, M. Sargon, Y. Sanli, H. Esme, and O. Ata. "P2.17-04 Imiquimod Attenuates Radiation-Induced Pulmonary Fibrosis." Journal of Thoracic Oncology 13, no. 10 (October 2018): S853. http://dx.doi.org/10.1016/j.jtho.2018.08.1530.

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Takemura, Naoki, Yosuke Kurashima, Yuki Mori, Kazuki Okada, Takayuki Ogino, Hideki Osawa, Hirosih Matsuno, et al. "Eosinophil depletion suppresses radiation-induced small intestinal fibrosis." Science Translational Medicine 10, no. 429 (February 21, 2018): eaan0333. http://dx.doi.org/10.1126/scitranslmed.aan0333.

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Zhang, KunYi, XuYu He, Yingling Zhou, Lijuan Gao, Zhengyu Qi, Jiyan Chen, and Xiuren Gao. "Atorvastatin Ameliorates Radiation-Induced Cardiac Fibrosis in Rats." Radiation Research 184, no. 6 (December 2015): 611–20. http://dx.doi.org/10.1667/rr14075.1.

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Wang, Jieqi, Arya M. Iranmanesh, and M. Elizabeth Oates. "Skeletal Scintigraphy in Radiation-Induced Fibrosis With Lymphedema." Clinical Nuclear Medicine 42, no. 3 (March 2017): 231–34. http://dx.doi.org/10.1097/rlu.0000000000001525.

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Straub, Jeffrey M., Jacob New, Chase D. Hamilton, Chris Lominska, Yelizaveta Shnayder, and Sufi M. Thomas. "Radiation-induced fibrosis: mechanisms and implications for therapy." Journal of Cancer Research and Clinical Oncology 141, no. 11 (April 25, 2015): 1985–94. http://dx.doi.org/10.1007/s00432-015-1974-6.

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Lee, Judy W., Richard H. Zoumalan, and Pierre Saadeh. "Radiation-Induced Fibrosis: A Rationale for Smad3 Inhibition." Otolaryngology–Head and Neck Surgery 141, no. 2_suppl (September 2009): P57. http://dx.doi.org/10.1016/j.otohns.2009.06.171.

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Sahu, Kamal Kant, Ajay Kumar Mishra, and Mohsen Noreldin. "A Challenging Case of Radiation-Induced Lung Fibrosis." American Journal of Medicine 133, no. 10 (October 2020): 1158–61. http://dx.doi.org/10.1016/j.amjmed.2020.03.018.

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Chiao, Teresa B., and Audrey J. Lee. "Role of Pentoxifylline and Vitamin E in Attenuation of Radiation-Induced Fibrosis." Annals of Pharmacotherapy 39, no. 3 (March 2005): 516–22. http://dx.doi.org/10.1345/aph.1e186.

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OBJECTIVE: To evaluate the use of pentoxifylline and vitamin E as monotherapy and in combination for the treatment of radiation-induced fibrosis (RIF). DATA SOURCES: Literature retrieval was performed through MEDLINE (1966–March 2004) using the terms vitamin E, α-tocopherol, pentoxifylline, radiation-induced fibrosis, and radiation injury. DATA SYNTHESIS: Few treatments exist for managing RIF of soft tissues. Due to its antioxidant properties, vitamin E may reduce the oxidative damage induced by radiation. The precise mechanism of action for pentoxifylline in management of RIF remains unclear. Uncontrolled studies evaluating vitamin E or pentoxifylline as monotherapy in RIF have shown modest improvement in clinical regression of fibrosis. However, controlled data are needed to verify these benefits. Studies involving pentoxifylline plus vitamin E demonstrated regression in RIF. The combination was more effective than placebo and may be superior to monotherapy with either agent. Adverse effects were rarely reported in the studies and consisted mainly of gastrointestinal and nervous system effects. CONCLUSIONS: Overall, pentoxifylline is well tolerated and is one of the few commercially available drugs with clinical data for management of RIF. Despite a lack of large, well-designed clinical trials, pentoxifylline plus vitamin E should be considered as an option in patients with symptomatic RIF.

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Jiang, Yifang, Fengming You, Jie Zhu, Chuan Zheng, Ran Yan, and Jinhao Zeng. "Cryptotanshinone Ameliorates Radiation-Induced Lung Injury in Rats." Evidence-Based Complementary and Alternative Medicine 2019 (February 20, 2019): 1–14. http://dx.doi.org/10.1155/2019/1908416.

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Cryptotanshinone (CTS) was reported to repress a variety of systemic inflammation and alleviate cardiac fibrosis, but it is still unclear whether CTS could prevent radiation-induced lung injury (RILI). Here, we investigated the effects and underlying mechanisms of CTS on a RILI rat model. Our data revealed that CTS could efficiently preserve pulmonary function in RILI rats and reduce early pulmonary inflammation infiltration elicited, along with marked decreased levels of IL-6 and IL-10. Moreover, we found that CTS is superior to prednisone in attenuating collagen deposition and pulmonary fibrosis, in parallel with a marked drop of HYP (a collagen indicator) and α-SMA (a myofibroblast marker). Mechanistically, CTS inhibited profibrotic signals TGF-β1 and NOX-4 expressions, while enhancing the levels of antifibrotic enzyme MMP-1 in lung tissues. It is noteworthy that CTS treatment, in consistent with trichrome staining analysis, exhibited a clear advantage over PND in enhancing MMP-1 levels. However, CTS exhibited little effect on CTGF activation and on COX-2 suppression. Finally, CTS treatment significantly mitigated the radiation-induced activation of CCL3 and its receptor CCR1. In summary, CTS treatment could attenuate RILI, especially pulmonary fibrosis, in rats. The regulation on production and release of inflammatory or fibrotic factors IL-6, IL-10, TGF-β1, NOX-4, and MMP-1, especially MMP-1 and inhibition on CCL3/CCR1 activation, may partly attribute to its attenuating RILI effect.

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Wang, Ping, Ziyan Yan, Ping-Kun Zhou, and Yongqing Gu. "The Promising Therapeutic Approaches for Radiation-Induced Pulmonary Fibrosis: Targeting Radiation-Induced Mesenchymal Transition of Alveolar Type II Epithelial Cells." International Journal of Molecular Sciences 23, no. 23 (November 30, 2022): 15014. http://dx.doi.org/10.3390/ijms232315014.

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Radiation-induced pulmonary fibrosis (RIPF) is a common consequence of radiation for thoracic tumors, and is accompanied by gradual and irreversible organ failure. This severely reduces the survival rate of cancer patients, due to the serious side effects and lack of clinically effective drugs and methods. Radiation-induced pulmonary fibrosis is a dynamic process involving many complicated and varied mechanisms, of which alveolar type II epithelial (AT2) cells are one of the primary target cells, and the epithelial–mesenchymal transition (EMT) of AT2 cells is very relevant in the clinical search for effective targets. Therefore, this review summarizes several important signaling pathways that can induce EMT in AT2 cells, and searches for molecular targets with potential effects on RIPF among them, in order to provide effective therapeutic tools for the clinical prevention and treatment of RIPF.

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