Involvement of Angiotensin II and Reactive Oxygen Species in Pancreatic Fibrosis

Sakurai, Toshiharu; Kudo, Masatoshi; Fukuta, N; Nakatani, Tatsuya; Kimura, Masatomo; Park, Ah-Mee; Munakata, Hiroshi

doi:10.1159/000323478

Cited by 33 publications

(22 citation statements)

References 32 publications

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“…A wide variety of agents have been identified that inhibit ECM production or the proliferation of PSCs, such as plant-derived polyphenol (green tea polyphenol, ellagic acid and curcumin) [101][102][103], NADPH oxidase inhibitor [48] and angiotensin II type 1 receptor blocker (ARB) [104]. Among these agents, ARB has been used clinically as an antihypertensive drug with acceptable feasibility and safety.…”

Section: Therapy-resistance and Stromal Cellsmentioning

confidence: 99%

Inflammation and pancreatic cancer: disease promoter and new therapeutic target

2013

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Chronic inflammation has a certain impact on the carcinogenesis of the digestive organs. The characteristic tissue structure of pancreatic cancer, desmoplasia, results from inflammatory processes induced by cancer cells and stromal cells. Concerning the progression of pancreatic cancer, recent research has clarified the pivotal role of tumorstromal interaction, which promotes the development of an invasive phenotype of cancer and provides survival advantages against chemotherapeutic agents or immune surveillance. Tumor stromal cells such as pancreatic stellate cells and immune cells establish a microenvironment that protects cancer cells through complex interactions. The microenvironment of pancreatic cancer acts as a niche for pancreatic cancer stem cells from which therapy-resistance and disease recurrence develop. Inhibition of the stromal functions or restoration of the immune reaction against cancer cells has therapeutic benefits that enhance the efficacy of conventional therapies. Some of the recent advances in this field are now under evaluation in clinical settings, but many problems must be overcome to establish a radical therapy for pancreatic cancer. This review summarizes current knowledge about the tumor-promoting stromal functions, immune system modulation and therapeutic strategies targeting tumorstromal interactions in pancreatic cancer.

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Section: Therapy-resistance and Stromal Cellsmentioning

confidence: 99%

Inflammation and pancreatic cancer: disease promoter and new therapeutic target

2013

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“…Presently, however, the specificity of this approach is unsatisfactory, and further improvements in equipments and techniques are anticipated. Although not directly related to pancreatic cancer, angiotensin-II and reactive oxygen species seem to be involved in the development of pancreatic fibrosis and hence pancreatic cancer, and this is therefore a topic that deserves attention [18] .…”

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confidence: 99%

Preface

Kudo

Yamao²,

Shimosegawa³

2011

Pancreatology

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“…There are many studies on the prevention of fibrosis by angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) (Tsang et al 2004). For example, we previously reported that treatment with ARBs and ACEI prevented the development of chronic pancreatitis and fibrosis in Wistar Bonn/ Kobori rats (Sakurai et al 2011). As mentioned above, angiotensin II also induces the production of ROS (Thakur et al 2010;Barnes and Gorin 2011).…”

Section: Potential Antifibrotic Therapiesmentioning

confidence: 98%

Myofibroblasts: Biochemical and Proteomic Approaches to Fibrosis

Honda

Park

Yoshida

et al. 2013

Tohoku J. Exp. Med.

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Fibrosis is a state, in which excess amounts of extracellular matrix are deposited in the tissue. Fibrosis can occur in various organs, including the liver, lung, kidney and heart. The progression of fibrosis involves interstitial hypercellularity, accumulation of extracellular matrix, and atrophy of epithelial structures, resulting in a loss of normal function. Myofibroblasts play a crucial role in the development and progress of fibrosis. When stimulated, myofibroblasts actively synthesize connective tissue components and cause organ fibrosis. As a result, the process and the mechanism of myofibroblast activation represent a target for antifibrotic treatment. As yet, however, an effective treatment has not been developed, and new treatment modalities are expected. Because activation of myofibroblasts is a key event during fibrosis development, there is great interest in identifying and characterizing proteins whose expression is changed after this activation. In this review, fibrosis is outlined and the role of myofibroblasts in this disorder is described. Furthermore, the search for candidate proteins to target for treatment and the prospects of antifibrotic therapy are discussed.

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Involvement of Angiotensin II and Reactive Oxygen Species in Pancreatic Fibrosis

Cited by 33 publications

References 32 publications

Inflammation and pancreatic cancer: disease promoter and new therapeutic target

Inflammation and pancreatic cancer: disease promoter and new therapeutic target

Preface

Myofibroblasts: Biochemical and Proteomic Approaches to Fibrosis

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