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10.1016/j.addr.2009.01.005 http://scihub22266oqcxt.onion/10.1016/j.addr.2009.01.005 19233238!2691416!19233238     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Adv+Drug+Deliv+Rev 2009 ; 61 (4): 351-63 Nephropedia Template TP {{tp|p=19233238|t=2009. Antioxidant enzyme gene transfer for ischemic diseases |pdf=|usr=}}{{19233238}} gab.com Text Antioxidant enzyme gene transfer for ischemic diseases JO: Adv Drug Deliv Rev http://www.kidney.de/pget.php?&tw=1&pmid=19233238 #FOAvip The balance of redox is pivotal for normal function and integrity of tissues. Ischemic insults occur as results of a variety of conditions, leading to an accumulation of reactive oxygen species (ROS) and an imbalanced redox status in the tissues. The oxidant stress may activate signaling mechanisms provoking more toxic events, and eventually cause tissue damage. Therefore, treatments with antioxidants, free radical scavengers and their mimetics, as well as gene transfer approaches to overexpress antioxidant genes represent potential therapeutic options to correct the redox imbalance. Among them, antioxidant gene transfer may enhance the production of antioxidant scavengers, and has been employed to experimentally prevent or treat ischemic injury in cardiovascular, pulmonary, hepatic, intestinal, central nervous or other systems in animal models. With improvements in vector systems and delivery approaches, innovative antioxidant gene therapy has conferred better outcomes for myocardial infarction, reduced restenosis after coronary angioplasty, improved the quality and function of liver grafts, as well as outcome of intestinal and cerebral ischemic attacks. However, it is crucial to be mindful that like other therapeutic armentarium, the efficacy of antioxidant gene transfer requires extensive preclinical investigation before it can be used in patients, and that it may have unanticipated short- or long-term adverse effects. Thus, it is critical to balance between the therapeutic benefits and potential risks, to develop disease-specific antioxidant gene transfer strategies, to deliver the therapy with an optimal time window and in a safe manner. This review attempts to provide the rationale, the most effective approaches and the potential hurdles of available antioxidant gene transfer approaches for ischemic injury in various organs, as well as the possible directions of future preclinical and clinical investigations of this highly promising therapeutic modality. Twit Text FOAVip Antioxidant enzyme gene transfer for ischemic diseases ????Adv Drug Deliv Rev http://www.kidney.de/pget.php?&tw=1&pmid=19233238 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19233238 #FOAvip English Wikipedia <ref>{{Cite pmid|19233238}}</ref> Antioxidant enzyme gene transfer for ischemic diseases #MMPMID19233238 Wu J; Hecker JG; Chiamvimonvat N Adv Drug Deliv Rev 2009[Apr]; 61 (4): 351-63 PMID19233238show ga The balance of redox is pivotal for normal function and integrity of tissues. Ischemic insults occur as results of a variety of conditions, leading to an accumulation of reactive oxygen species (ROS) and an imbalanced redox status in the tissues. The oxidant stress may activate signaling mechanisms provoking more toxic events, and eventually cause tissue damage. Therefore, treatments with antioxidants, free radical scavengers and their mimetics, as well as gene transfer approaches to overexpress antioxidant genes represent potential therapeutic options to correct the redox imbalance. Among them, antioxidant gene transfer may enhance the production of antioxidant scavengers, and has been employed to experimentally prevent or treat ischemic injury in cardiovascular, pulmonary, hepatic, intestinal, central nervous or other systems in animal models. With improvements in vector systems and delivery approaches, innovative antioxidant gene therapy has conferred better outcomes for myocardial infarction, reduced restenosis after coronary angioplasty, improved the quality and function of liver grafts, as well as outcome of intestinal and cerebral ischemic attacks. However, it is crucial to be mindful that like other therapeutic armentarium, the efficacy of antioxidant gene transfer requires extensive preclinical investigation before it can be used in patients, and that it may have unanticipated short- or long-term adverse effects. Thus, it is critical to balance between the therapeutic benefits and potential risks, to develop disease-specific antioxidant gene transfer strategies, to deliver the therapy with an optimal time window and in a safe manner. This review attempts to provide the rationale, the most effective approaches and the potential hurdles of available antioxidant gene transfer approaches for ischemic injury in various organs, as well as the possible directions of future preclinical and clinical investigations of this highly promising therapeutic modality. |*Gene Transfer Techniques/trends[MESH] |Animals[MESH] |Antioxidants/*administration & dosage[MESH] |Genetic Therapy/methods/trends[MESH] |Humans[MESH] |Ischemia/*enzymology/*genetics/therapy[MESH] |Oxidative Stress/drug effects/genetics[MESH]Antioxidant enzyme gene transfer for ischemic diseases (epmc).pdf DeepDyve Pubget Overpricing