Blog
About

4
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

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

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Most cited references 54

          • Record: found
          • Abstract: found
          • Article: not found

          Eukaryotic evolution, changes and challenges.

          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.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Oxidative damage and mitochondrial decay in aging.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              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.
                Bookmark

                Author and article information

                Journal
                NEP
                Nephron Physiol
                10.1159/issn.1660-2137
                Nephron Physiology
                S. Karger AG
                1660-2137
                2007
                December 2006
                08 November 2006
                : 105
                : 1
                : p1-p10
                Affiliations
                Centre for Nephrology and Department of Physiology (Epithelial Transport and Cell Biology Group), Royal Free and University College Medical School, London, UK
                Article
                96860 Nephron Physiol 2007;105:p1–p10
                10.1159/000096860
                17095876
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 1, References: 69, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/96860
                Categories
                Minireview

                Comments

                Comment on this article