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      Mechanisms of Biliary Damage

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          Abstract

          Bile duct damage is present in virtually all cholangiopathies, which share the biliary epithelial cells (i.e. cholangiocytes) as a common pathogenic target. Cholangiocyte cell death largely occurs through the process of apoptosis. In this review, we will summarize the mechanisms through which biliary damage occurs in a variety of animal and in vitro models, such as extrahepatic cholestasis induced by bile duct ligation (BDL), cytotoxin- and hepatotoxin-induced liver injury, and biliary atresia. Although we have increased our knowledge of the factors that regulate cholangiocyte cell death mechanisms during cholangiopathies, especially in experimental models, there is still a lack of effective treatment modalities for these biliary disorders. However, future studies will hopefully provide for new therapeutic modalities for the prevention or restoration of biliary mass and function lost during the progression of cholangiopathies.

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          Most cited references76

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          Cell death: critical control points.

          Programmed cell death is a distinct genetic and biochemical pathway essential to metazoans. An intact death pathway is required for successful embryonic development and the maintenance of normal tissue homeostasis. Apoptosis has proven to be tightly interwoven with other essential cell pathways. The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics.
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            Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy.

            Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.
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              Lysosomes and autophagy in cell death control.

              Lysosomal hydrolases participate in the digestion of endocytosed and autophagocytosed material inside the lysosomal/autolysosomal compartment in acute cell death when released into the cytosol and in cancer progression following their release into the extracellular space. Lysosomal alterations are common in cancer cells. The increased expression and altered trafficking of lysosomal enzymes participates in tissue invasion, angiogenesis and sensitization to the lysosomal death pathway. But lysosomal heat-shock protein 70 locally prevents lysosomal-membrane permeabilization. Similarly, alterations in the autophagic compartment are linked to carcinogenesis and resistance to chemotherapy. Targeting these pathways might constitute a novel approach to cancer therapy.
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                Author and article information

                Journal
                J Cell Death
                J Cell Death
                Journal of Cell Death
                Journal of Cell Death
                Libertas Academica
                1179-0660
                2010
                17 March 2010
                : 3
                : 13-21
                Affiliations
                [1 ]Digestive Disease Research Center, Scott & White
                [2 ]Department of Medicine, Scott & White and Texas A&M Health Science Center, College of Medicine, Temple, Texas.
                [3 ]Central Texas Veterans Health Care System, Temple, Texas.
                [4 ]Shengjing Hospital, China Medical University, Shenyang City, Liaoning Province, China.
                [5 ]Human Anatomy, University of Rome “La Sapienza”, Rome, Italy.
                [6 ]Experimental Medicine, University of L’Aquila, L’Aquila, Italy.
                Author notes
                Article
                cld-3-013
                10.4137/JCD.S2785
                3424638
                22924014
                1ded5e96-b8e2-44cc-8917-959cd6f2bf37
                © 2010 the author(s), publisher and licensee Libertas Academica Ltd.

                This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.

                History
                Categories
                Review

                cholangiocyte,cholangiocarcinoma,apoptosis,cholestatic liver diseases

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