Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders
Sirtuins (SIRT1–SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD + levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modul...
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| Veröffentlicht in: | Neurochemical research 2017-03, Vol.42 (3), p.876-890 |
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| creator | Jęśko, Henryk Wencel, Przemysław Strosznajder, Robert P. Strosznajder, Joanna B. |
| description | Sirtuins (SIRT1–SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD
+
levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD
+
-dependent post-translational protein modifiers. The cross-talk between SIRTs TFs and PARPs is a highly promising research target in a number of brain pathologies. This review describes updated results on sirtuins in brain aging/neurodegeneration. It focuses on SIRT1 but also on the roles of mitochondrial SIRTs (SIRT3, 4, 5) and on SIRT6 and SIRT2 localized in the nucleus and in cytosol, respectively. The involvement of SIRTs in regulation of insulin-like growth factor signaling in the brain during aging and in Alzheimer’s disease was also focused. Moreover, we analyze the mechanism(s) and potential significance of interactions between SIRTs and several TFs in the regulation of cell survival and death. A critical view is given on the application of SIRT activators/modulators in therapy of neurodegenerative diseases. |
| doi_str_mv | 10.1007/s11064-016-2110-y |
| format | Article |
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+
levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD
+
-dependent post-translational protein modifiers. The cross-talk between SIRTs TFs and PARPs is a highly promising research target in a number of brain pathologies. This review describes updated results on sirtuins in brain aging/neurodegeneration. It focuses on SIRT1 but also on the roles of mitochondrial SIRTs (SIRT3, 4, 5) and on SIRT6 and SIRT2 localized in the nucleus and in cytosol, respectively. The involvement of SIRTs in regulation of insulin-like growth factor signaling in the brain during aging and in Alzheimer’s disease was also focused. Moreover, we analyze the mechanism(s) and potential significance of interactions between SIRTs and several TFs in the regulation of cell survival and death. A critical view is given on the application of SIRT activators/modulators in therapy of neurodegenerative diseases.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-016-2110-y</identifier><identifier>PMID: 27882448</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aging - metabolism ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain - metabolism ; Cell Biology ; Cell Death ; Cell Nucleus - metabolism ; Cell Survival ; Cytosol - metabolism ; Energy Metabolism ; Humans ; Mitochondria - metabolism ; Neurochemistry ; Neurodegenerative Diseases - drug therapy ; Neurodegenerative Diseases - metabolism ; Neurology ; Neuroprotection ; Neuroprotective Agents - therapeutic use ; Neurosciences ; Original Paper ; Signal Transduction ; Sirtuins - metabolism ; Somatomedins - metabolism ; Transcription Factors - metabolism</subject><ispartof>Neurochemical research, 2017-03, Vol.42 (3), p.876-890</ispartof><rights>The Author(s) 2016</rights><rights>Neurochemical Research is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-8978e0201310cb45c991b9e2f53b6a7f7e62a5517f99cc3259f8cba53a8793103</citedby><cites>FETCH-LOGICAL-c503t-8978e0201310cb45c991b9e2f53b6a7f7e62a5517f99cc3259f8cba53a8793103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-016-2110-y$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-016-2110-y$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,778,782,883,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27882448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jęśko, Henryk</creatorcontrib><creatorcontrib>Wencel, Przemysław</creatorcontrib><creatorcontrib>Strosznajder, Robert P.</creatorcontrib><creatorcontrib>Strosznajder, Joanna B.</creatorcontrib><title>Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Sirtuins (SIRT1–SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD
+
levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD
+
-dependent post-translational protein modifiers. The cross-talk between SIRTs TFs and PARPs is a highly promising research target in a number of brain pathologies. This review describes updated results on sirtuins in brain aging/neurodegeneration. It focuses on SIRT1 but also on the roles of mitochondrial SIRTs (SIRT3, 4, 5) and on SIRT6 and SIRT2 localized in the nucleus and in cytosol, respectively. The involvement of SIRTs in regulation of insulin-like growth factor signaling in the brain during aging and in Alzheimer’s disease was also focused. Moreover, we analyze the mechanism(s) and potential significance of interactions between SIRTs and several TFs in the regulation of cell survival and death. A critical view is given on the application of SIRT activators/modulators in therapy of neurodegenerative diseases.</description><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - metabolism</subject><subject>Cell Biology</subject><subject>Cell Death</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell Survival</subject><subject>Cytosol - metabolism</subject><subject>Energy Metabolism</subject><subject>Humans</subject><subject>Mitochondria - metabolism</subject><subject>Neurochemistry</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Signal Transduction</subject><subject>Sirtuins - metabolism</subject><subject>Somatomedins - metabolism</subject><subject>Transcription Factors - metabolism</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkVtLHDEYhoO06HbrD_CmDPTGm2lzmJxuBA-tFaSCh-uQyX4zRmYTTWaE_ffNula0IPQmCbzP-x3yIrRH8DeCsfyeCcGiqTERNS3PerWFZoRLVguN2Qc0w6yojGi8gz7lfIdxcVGyjXaoVIo2jZqh0yufxsmHXNmwqK5vwafqMg6QKx-qo2TLedj70D_Jv2FKcQE9BEh29I9Qnfgc0wJS_ow-dnbIsPt8z9HNzx_Xx7_q84vTs-PD89pxzMZaaakAU0wYwa5tuNOatBpox1krrOwkCGo5J7LT2jlGue6Uay1nVkldPGyODjZ176d2CQsHYUx2MPfJL21amWi9easEf2v6-Gg445KXvnO0_1wgxYcJ8miWPjsYBhsgTtkQpYgUXGj2H2jDtBBa04J-_Qe9i1MK5ScKVSaXBV0PTzaUSzHnBN3L3ASbdaJmk6gpiZp1omZVPF9eL_zi-BthAegGyEUKPaRXrd-t-gcOt6rg</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Jęśko, Henryk</creator><creator>Wencel, Przemysław</creator><creator>Strosznajder, Robert P.</creator><creator>Strosznajder, Joanna B.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170301</creationdate><title>Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders</title><author>Jęśko, Henryk ; Wencel, Przemysław ; Strosznajder, Robert P. ; Strosznajder, Joanna B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-8978e0201310cb45c991b9e2f53b6a7f7e62a5517f99cc3259f8cba53a8793103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - metabolism</topic><topic>Cell Biology</topic><topic>Cell Death</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell Survival</topic><topic>Cytosol - metabolism</topic><topic>Energy Metabolism</topic><topic>Humans</topic><topic>Mitochondria - metabolism</topic><topic>Neurochemistry</topic><topic>Neurodegenerative Diseases - drug therapy</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Signal Transduction</topic><topic>Sirtuins - metabolism</topic><topic>Somatomedins - metabolism</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jęśko, Henryk</creatorcontrib><creatorcontrib>Wencel, Przemysław</creatorcontrib><creatorcontrib>Strosznajder, Robert P.</creatorcontrib><creatorcontrib>Strosznajder, Joanna B.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jęśko, Henryk</au><au>Wencel, Przemysław</au><au>Strosznajder, Robert P.</au><au>Strosznajder, Joanna B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>42</volume><issue>3</issue><spage>876</spage><epage>890</epage><pages>876-890</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Sirtuins (SIRT1–SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD
+
levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD
+
-dependent post-translational protein modifiers. The cross-talk between SIRTs TFs and PARPs is a highly promising research target in a number of brain pathologies. This review describes updated results on sirtuins in brain aging/neurodegeneration. It focuses on SIRT1 but also on the roles of mitochondrial SIRTs (SIRT3, 4, 5) and on SIRT6 and SIRT2 localized in the nucleus and in cytosol, respectively. The involvement of SIRTs in regulation of insulin-like growth factor signaling in the brain during aging and in Alzheimer’s disease was also focused. Moreover, we analyze the mechanism(s) and potential significance of interactions between SIRTs and several TFs in the regulation of cell survival and death. A critical view is given on the application of SIRT activators/modulators in therapy of neurodegenerative diseases.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27882448</pmid><doi>10.1007/s11064-016-2110-y</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neurochemical research, 2017-03, Vol.42 (3), p.876-890 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Aging - metabolism Animals Biochemistry Biomedical and Life Sciences Biomedicine Brain - metabolism Cell Biology Cell Death Cell Nucleus - metabolism Cell Survival Cytosol - metabolism Energy Metabolism Humans Mitochondria - metabolism Neurochemistry Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - metabolism Neurology Neuroprotection Neuroprotective Agents - therapeutic use Neurosciences Original Paper Signal Transduction Sirtuins - metabolism Somatomedins - metabolism Transcription Factors - metabolism |
| title | Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders |
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