Cytokine and anti-cytokine therapies in prevention or treatment of fibrosis in IBD

Jacob, Noam; Targan, Stephan R.; Shih, David Q.

doi:10.1177/2050640616649356

Cited by 18 publications

(11 citation statements)

References 107 publications

(182 reference statements)

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“…91 Although to the best of our knowledge their role in the development of NET-related fibrosis has not been investigated to date, prostaglandins and interleukins are known to play a role in the development and maintenance of chronic inflammation and to act as profibrotic molecules. 156,157…”

Section: Kinins and Other Peptidesmentioning

confidence: 99%

Neuroendocrine tumors and fibrosis: An unsolved mystery?

Laskaratos

Rombouts

Caplin

et al. 2017

Cancer

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Neuroendocrine tumors are a heterogeneous group of slow-growing neoplasms arising mainly from the enterochromaffin cells of the digestive and respiratory tract. Although they are relatively rare, their incidence is rising. It has long been observed that they often are associated with the development of fibrosis, both local and distant. Fibrotic complications, such as carcinoid heart disease and mesenteric desmoplasia, may lead to considerable morbidity or even affect prognosis. The elucidation of the pathophysiology of fibrosis would be of critical importance for the development of targeted therapeutic strategies. In this article, the authors review the available evidence regarding the biological basis of fibrosis in neuroendocrine tumors. They explore the role of the tumor microenvironment and the interplay between tumor cells and fibroblasts as a key factor in fibrogenesis and tumor development/progression. They also review the role of serotonin, growth factors, and other peptides in the development of carcinoid-related fibrotic reactions. Cancer 2017;123:4770-90. © 2017 American Cancer Society.

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Section: Kinins and Other Peptidesmentioning

confidence: 99%

Neuroendocrine tumors and fibrosis: An unsolved mystery?

Laskaratos

Rombouts

Caplin

et al. 2017

Cancer

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“…Intestinal fibrosis is a major complication of inflammatory bowel disease (IBD) and can occur in both ulcerative colitis (UC) and CD, but is much more prevalent in CD ( 3 ). Approximately 40% of CD patients with ileal disease develop clinically apparent strictures throughout their lifetime, which significantly influences the quality of life ( 4 , 5 ). The excessive presence of fibrous tissue increases the thickness of bowel wall, reducing the elasticity and the function over the affected area.…”

Section: Intestinal Fibroblast/myofibroblast and Fibrosismentioning

confidence: 99%

Significant contribution of TRPC6 channel-mediated Ca<sup>2+</sup> influx to the pathogenesis of Crohn’s disease fibrotic stenosis

Kurahara

Hiraishi

Sumiyoshi

et al. 2016

J. Smooth Muscle Res.

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Intestinal fibrosis is an intractable complication of Crohn's disease (CD), and, when occurring excessively, causes severe intestinal obstruction that often necessitates surgical resection. The fibrosis is characterized by an imbalance in the turnover of extracellular matrix (ECM) components, where intestinal fibroblasts/myofibroblasts play active roles in ECM production, fibrogenesis and tissue remodeling, which eventually leads to the formation of stenotic lesions. There is however a great paucity of knowledge about how intestinal fibrosis initiates and progresses, which hampers the development of effective pharmacotherapies against CD. Recently, we explored the potential implications of transient receptor potential (TRP) channels in the pathogenesis of intestinal fibrosis, since they are known to act as cellular stress sensors/transducers affecting intracellular Ca2+ homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling. In this review, we will place a particular emphasis on the intestinal fibroblast/myofibroblast TRPC6 channel to discuss its modulatory effects on fibrotic responses and therapeutic potential for anti-fibrotic treatment against CD-related stenosis.

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“…Myofibroblasts possess increased contractile properties with expression of alpha smooth muscle actin (α-SMA) and non-muscle myosins. Transforming growth factor-β1 (TGF-β1) is the best recognized inducer of myofibroblasts differentiation (5); others include environmental stimuli such as hypoxia (6), and other cytokines (7). In normal wound healing, myofibroblasts disappear through apoptosis, and the ECM at the wound site eventually get reabsorbed (8).…”

Section: Introductionmentioning

confidence: 99%

DNA methylation regulated gene expression in organ fibrosis

Zhang

Lyu

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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DNA methylation is a major epigenetic mechanism to regulate gene expression. Epigenetic regulation, including DNA methylation, histone modifications and RNA interference, results in heritable changes in gene expression independent of alterations in DNA sequence. Epigenetic regulation often occurs in response to aging and environment stimuli, including exposures and diet. Studies have shown that DNA methylation is critical in the pathogenesis of fibrosis involving multiple organs sytems, contributing to significant morbidity and mortality. Aberrant DNA methylation can silence or activate gene expression patterns that drive the fibrosis process. Fibrosis is a pathological wound healing process in response to chronic injury. It is characterized by excessive extracellular matrix production and accumulation, which eventually affects organ architecture and results in organ failure. Fibrosis can affect a wide range of organs, including the heart and lungs, and have limited therapeutic options. DNA methylation, like other epigenetic process, is reversible, therefore regarded as attractive therapeutic interventions. Although epigenetic mechanisms are highly interactive and often reinforcing, this review discusses DNA methylation-dependent mechanisms in the pathogenesis of organ fibrosis, with focus on cardiac and pulmonary fibrosis. We discuss specific pro- and anti-fibrotic genes and pathways regulated by DNA methylation in organ fibrosis; we further highlight the potential benefits and side-effects of epigenetic therapies in fibrotic disorders.

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Cytokine and anti-cytokine therapies in prevention or treatment of fibrosis in IBD

Cited by 18 publications

References 107 publications

Neuroendocrine tumors and fibrosis: An unsolved mystery?

Neuroendocrine tumors and fibrosis: An unsolved mystery?

Significant contribution of TRPC6 channel-mediated Ca<sup>2+</sup> influx to the pathogenesis of Crohn’s disease fibrotic stenosis

DNA methylation regulated gene expression in organ fibrosis

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