For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
0
views
91
references
 Top references
cited by
4
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      339
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Sirtuins play critical and diverse roles in acute kidney injury

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      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

          Acute kidney injury (AKI) is an extremely common medical affliction affecting both adult and pediatric patients resulting from hypoxic, nephrotoxic, and septic insults affecting approximately 20% of all hospital patients and up to 50% of patients in the intensive care unit. There are currently no therapeutics for patients who suffer AKI. Much recent work has focused on designing and implementing therapeutics for AKI. This review focuses on a family of enzymes known as sirtuins that play critical roles in regulating many cellular and biological functions. There are 7 mammalian sirtuins (SIRT1–7) that play roles in regulating the acylation of a wide variety of pathways. Furthermore, all but one of the mammalian sirtuins have been shown to play critical roles in mediating AKI based on preclinical studies. These diverse enzymes show exciting potential for therapeutic manipulation. This review will focus on the specific roles of each of the investigated sirtuins and the potential for manipulation of the various sirtuins and their effector pathways in mediating kidney injury.

          Related collections

          Most cited references91

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

          Sirtuins in mammals: insights into their biological function.

          Shaday Michan, David. Sinclair (2007)
          Sirtuins are a conserved family of proteins found in all domains of life. The first known sirtuin, Sir2 (silent information regulator 2) of Saccharomyces cerevisiae, from which the family derives its name, regulates ribosomal DNA recombination, gene silencing, DNA repair, chromosomal stability and longevity. Sir2 homologues also modulate lifespan in worms and flies, and may underlie the beneficial effects of caloric restriction, the only regimen that slows aging and extends lifespan of most classes of organism, including mammals. Sirtuins have gained considerable attention for their impact on mammalian physiology, since they may provide novel targets for treating diseases associated with aging and perhaps extend human lifespan. In this review we describe our current understanding of the biological function of the seven mammalian sirtuins, SIRT1-7, and we will also discuss their potential as mediators of caloric restriction and as pharmacological targets to delay and treat human age-related diseases.
          Article 0 comments Cited 501 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1.

            Bruce M Spiegelman, Wilhelm Haas, Christopher Rodgers … (2005)
            Homeostatic mechanisms in mammals respond to hormones and nutrients to maintain blood glucose levels within a narrow range. Caloric restriction causes many changes in glucose metabolism and extends lifespan; however, how this metabolism is connected to the ageing process is largely unknown. We show here that the Sir2 homologue, SIRT1--which modulates ageing in several species--controls the gluconeogenic/glycolytic pathways in liver in response to fasting signals through the transcriptional coactivator PGC-1alpha. A nutrient signalling response that is mediated by pyruvate induces SIRT1 protein in liver during fasting. We find that once SIRT1 is induced, it interacts with and deacetylates PGC-1alpha at specific lysine residues in an NAD(+)-dependent manner. SIRT1 induces gluconeogenic genes and hepatic glucose output through PGC-1alpha, but does not regulate the effects of PGC-1alpha on mitochondrial genes. In addition, SIRT1 modulates the effects of PGC-1alpha repression of glycolytic genes in response to fasting and pyruvate. Thus, we have identified a molecular mechanism whereby SIRT1 functions in glucose homeostasis as a modulator of PGC-1alpha. These findings have strong implications for the basic pathways of energy homeostasis, diabetes and lifespan.
            Article 0 comments Cited 341 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Pathophysiology of acute kidney injury.

              David P Basile, Melissa Anderson, Timothy A. Sutton (2012)
              Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia, or nephrotoxicity. An underlying feature is a rapid decline in glomerular filtration rate (GFR) usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or chronic kidney disease (CKD) patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future. © 2012 American Physiological Society. Compr Physiol 2:1303-1353, 2012.
              Article 0 comments Cited 339 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Sunder Sims-Lucas: simslucass@upmc.edu
                Journal
                Journal ID (nlm-ta): Pediatr Nephrol
                Journal ID (iso-abbrev): Pediatr Nephrol
                Title: Pediatric Nephrology (Berlin, Germany)
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 0931-041X
                ISSN (Electronic): 1432-198X
                Publication date (Electronic): 7 January 2021
                Pages: 1-8
                Affiliations
                [1 ]GRID grid.21925.3d, ISNI 0000 0004 1936 9000, Department of Pediatrics, Division of Nephrology, , University of Pittsburgh School of Medicine, ; Pittsburgh, PA USA
                [2 ]GRID grid.21925.3d, ISNI 0000 0004 1936 9000, Department of Pediatrics, Division of Medical Genetics, , University of Pittsburgh School of Medicine, ; Pittsburgh, PA USA
                [3 ]GRID grid.412689.0, ISNI 0000 0001 0650 7433, Division of Nephrology, Department of Pediatrics, , UPMC Children’s Hospital of Pittsburgh, Rangos Research Center, ; 4401 Penn Ave, Pittsburgh, PA 15224 USA
                Article
                Publisher ID: 4866
                DOI: 10.1007/s00467-020-04866-z
                PMC ID: 7788193
                PubMed ID: 33411071
                SO-VID: a2fcc86f-68d7-4010-bbfb-908eade76983
                Copyright © © IPNA 2021
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date received : 15 July 2020
                Date revision received : 8 October 2020
                Date accepted : 17 November 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000062, National Institute of Diabetes and Digestive and Kidney Diseases;
                Award ID: DK121758
                Award ID: DK125015
                Award ID: DK090242
                Award Recipient :
                Categories
                Subject: Review

                ScienceOpen disciplines: Nephrology
                Keywords: acute kidney injury,aki,sirtuins,acylation,therapy,metabolism
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: acute kidney injury, aki, sirtuins, acylation, therapy, metabolism

                Comments

                Comment on this article

                scite_

                Similar content339

                See all similar

                Cited by4

                See all cited by

                Most referenced authors1,447

                See all reference authors