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      The Not So ‘Mighty Chondrion’: Emergence of Renal Diseases due to Mitochondrial Dysfunction

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          Mitochondria are intracellular organelles with a variety of vital functions, including the provision of energy in the form of adenosine 5′-triphosphate. Increasingly, we are becoming more aware of the importance of mitochondrial dysfunction in a number of common medical conditions. In this review and overview, we focus on the growing evidence that mitochondrial dysfunction is involved in either the etiology or underlying pathophysiology of a broad spectrum of renal diseases, including acute renal injury due to ischemia-reperfusion injury, renal Fanconi syndrome, and glomerular disorders such as focal segmental glomerulosclerosis. In addition, mitochondrial dysfunction may also contribute to the growing burden of chronic kidney disease seen in our aging population, which is still largely unexplained. Unfortunately, at present, our ability to diagnose and treat renal disorders related to mitochondrial dysfunction is limited, and further work in this field is needed.

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          Most cited references 54

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          The idea that some eukaryotes primitively lacked mitochondria and were true intermediates in the prokaryote-to-eukaryote transition was an exciting prospect. It spawned major advances in understanding anaerobic and parasitic eukaryotes and those with previously overlooked mitochondria. But the evolutionary gap between prokaryotes and eukaryotes is now deeper, and the nature of the host that acquired the mitochondrion more obscure, than ever before.
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              Emerging biological roles for erythropoietin in the nervous system.

              Erythropoietin mediates an evolutionarily conserved, ancient immune response that limits damage to the heart, the nervous system and other tissues following injury. New evidence indicates that erythropoietin specifically prevents the destruction of viable tissue surrounding the site of an injury by signalling through a non-haematopoietic receptor. Engineered derivatives of erythropoietin that have a high affinity for this receptor have been developed, and these show robust tissue-protective effects in diverse preclinical models without stimulating erythropoiesis. A recent successful proof-of-concept clinical trial that used erythropoietin to treat human patients who had suffered a stroke encourages the evaluation of both this cytokine and non-erythropoietic derivatives as therapeutic agents to limit tissue injury.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                December 2006
                08 November 2006
                : 105
                : 1
                : p1-p10
                Centre for Nephrology and Department of Physiology (Epithelial Transport and Cell Biology Group), Royal Free and University College Medical School, London, UK
                96860 Nephron Physiol 2007;105:p1–p10
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 1, References: 69, Pages: 1
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