Novel Role of the SIRT1 in Endocrine and Metabolic Diseases

Silent information regulator 1 (SIRT1), a highly conserved NAD -dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development...

Full description

Saved in:
Bibliographic Details
Published in:International journal of biological sciences Vol. 19; no. 2; pp. 484 - 501
Main Authors: Lu, Chenxi, Zhao, Huadong, Liu, Yanqing, Yang, Zhi, Yao, Hairong, Liu, Tong, Gou, Tiantian, Wang, Li, Zhang, Juan, Tian, Ye, Yang, Yang, Zhang, Huan
Format: Journal Article
Language:English
Published: Australia Ivyspring International Publisher Pty Ltd 2023
Ivyspring International Publisher
Subjects:
ISSN:1449-2288, 1449-2288
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract Silent information regulator 1 (SIRT1), a highly conserved NAD -dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development of endocrine and metabolic diseases. In a variety of organisms, SIRT1 regulates gene expression through the deacetylation of histone, transcription factors, and lysine residues of other modified proteins including several metabolic and endocrine signal transcription factors, thereby enhancing the therapeutic effects of endocrine and metabolic diseases. These evidences indicate that targeting SIRT1 has promising applications in the treatment of endocrine and metabolic diseases. This review focuses on the role of SIRT1 in endocrine and metabolic diseases. First, we describe the background and structure of SIRT1. Then, we outline the role of SIRT1 in endocrine and metabolic diseases such as hyperuricemia, diabetes, hypertension, hyperlipidemia, osteoporosis, and polycystic ovarian syndrome. Subsequently, the SIRT1 agonists and inhibitors in the above diseases are summarized and future research directions are proposed. Overall, the information presents here may highlight the potential of SIRT1 as a future biomarker and therapeutic target for endocrine and metabolic diseases.
AbstractList Silent information regulator 1 (SIRT1), a highly conserved NAD+-dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development of endocrine and metabolic diseases. In a variety of organisms, SIRT1 regulates gene expression through the deacetylation of histone, transcription factors, and lysine residues of other modified proteins including several metabolic and endocrine signal transcription factors, thereby enhancing the therapeutic effects of endocrine and metabolic diseases. These evidences indicate that targeting SIRT1 has promising applications in the treatment of endocrine and metabolic diseases. This review focuses on the role of SIRT1 in endocrine and metabolic diseases. First, we describe the background and structure of SIRT1. Then, we outline the role of SIRT1 in endocrine and metabolic diseases such as hyperuricemia, diabetes, hypertension, hyperlipidemia, osteoporosis, and polycystic ovarian syndrome. Subsequently, the SIRT1 agonists and inhibitors in the above diseases are summarized and future research directions are proposed. Overall, the information presents here may highlight the potential of SIRT1 as a future biomarker and therapeutic target for endocrine and metabolic diseases.
Silent information regulator 1 (SIRT1), a highly conserved NAD+-dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development of endocrine and metabolic diseases. In a variety of organisms, SIRT1 regulates gene expression through the deacetylation of histone, transcription factors, and lysine residues of other modified proteins including several metabolic and endocrine signal transcription factors, thereby enhancing the therapeutic effects of endocrine and metabolic diseases. These evidences indicate that targeting SIRT1 has promising applications in the treatment of endocrine and metabolic diseases. This review focuses on the role of SIRT1 in endocrine and metabolic diseases. First, we describe the background and structure of SIRT1. Then, we outline the role of SIRT1 in endocrine and metabolic diseases such as hyperuricemia, diabetes, hypertension, hyperlipidemia, osteoporosis, and polycystic ovarian syndrome. Subsequently, the SIRT1 agonists and inhibitors in the above diseases are summarized and future research directions are proposed. Overall, the information presents here may highlight the potential of SIRT1 as a future biomarker and therapeutic target for endocrine and metabolic diseases.Silent information regulator 1 (SIRT1), a highly conserved NAD+-dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development of endocrine and metabolic diseases. In a variety of organisms, SIRT1 regulates gene expression through the deacetylation of histone, transcription factors, and lysine residues of other modified proteins including several metabolic and endocrine signal transcription factors, thereby enhancing the therapeutic effects of endocrine and metabolic diseases. These evidences indicate that targeting SIRT1 has promising applications in the treatment of endocrine and metabolic diseases. This review focuses on the role of SIRT1 in endocrine and metabolic diseases. First, we describe the background and structure of SIRT1. Then, we outline the role of SIRT1 in endocrine and metabolic diseases such as hyperuricemia, diabetes, hypertension, hyperlipidemia, osteoporosis, and polycystic ovarian syndrome. Subsequently, the SIRT1 agonists and inhibitors in the above diseases are summarized and future research directions are proposed. Overall, the information presents here may highlight the potential of SIRT1 as a future biomarker and therapeutic target for endocrine and metabolic diseases.
Silent information regulator 1 (SIRT1), a highly conserved NAD -dependent deacetylase, is a cellular regulator that has received extensive attention in recent years and regarded as a sensor of cellular energy and metabolism. The accumulated evidence suggests that SIRT1 is involved in the development of endocrine and metabolic diseases. In a variety of organisms, SIRT1 regulates gene expression through the deacetylation of histone, transcription factors, and lysine residues of other modified proteins including several metabolic and endocrine signal transcription factors, thereby enhancing the therapeutic effects of endocrine and metabolic diseases. These evidences indicate that targeting SIRT1 has promising applications in the treatment of endocrine and metabolic diseases. This review focuses on the role of SIRT1 in endocrine and metabolic diseases. First, we describe the background and structure of SIRT1. Then, we outline the role of SIRT1 in endocrine and metabolic diseases such as hyperuricemia, diabetes, hypertension, hyperlipidemia, osteoporosis, and polycystic ovarian syndrome. Subsequently, the SIRT1 agonists and inhibitors in the above diseases are summarized and future research directions are proposed. Overall, the information presents here may highlight the potential of SIRT1 as a future biomarker and therapeutic target for endocrine and metabolic diseases.
Author Lu, Chenxi
Zhang, Juan
Zhang, Huan
Wang, Li
Yao, Hairong
Liu, Tong
Zhao, Huadong
Gou, Tiantian
Tian, Ye
Liu, Yanqing
Yang, Yang
Yang, Zhi
AuthorAffiliation 2 Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. Faculty of Life Sciences and Medicine, Northwest University, Xi'an, China
1 Department of Cardiology, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University. Faculty of Life Sciences and Medicine, Northwest University, Xi'an, China
3 Department of General Surgery, Tangdu Hospital, The Airforce Medical University, 1 Xinsi Road, Xi'an 710038, China
AuthorAffiliation_xml – name: 1 Department of Cardiology, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University. Faculty of Life Sciences and Medicine, Northwest University, Xi'an, China
– name: 3 Department of General Surgery, Tangdu Hospital, The Airforce Medical University, 1 Xinsi Road, Xi'an 710038, China
– name: 2 Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. Faculty of Life Sciences and Medicine, Northwest University, Xi'an, China
Author_xml – sequence: 1
  givenname: Chenxi
  surname: Lu
  fullname: Lu, Chenxi
– sequence: 2
  givenname: Huadong
  surname: Zhao
  fullname: Zhao, Huadong
– sequence: 3
  givenname: Yanqing
  surname: Liu
  fullname: Liu, Yanqing
– sequence: 4
  givenname: Zhi
  surname: Yang
  fullname: Yang, Zhi
– sequence: 5
  givenname: Hairong
  surname: Yao
  fullname: Yao, Hairong
– sequence: 6
  givenname: Tong
  surname: Liu
  fullname: Liu, Tong
– sequence: 7
  givenname: Tiantian
  surname: Gou
  fullname: Gou, Tiantian
– sequence: 8
  givenname: Li
  surname: Wang
  fullname: Wang, Li
– sequence: 9
  givenname: Juan
  surname: Zhang
  fullname: Zhang, Juan
– sequence: 10
  givenname: Ye
  surname: Tian
  fullname: Tian, Ye
– sequence: 11
  givenname: Yang
  surname: Yang
  fullname: Yang, Yang
– sequence: 12
  givenname: Huan
  surname: Zhang
  fullname: Zhang, Huan
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36632457$$D View this record in MEDLINE/PubMed
BookMark eNptkVtLwzAYhoNMdB5u_AES8EaEaZK2aYIgyDzCVPBwHdL0i8voktm0A_-9rSdUvEogz_fyfHk30MAHDwjtUHKY04wcuVkRD3PBs3QFDWmayhFjQgx-3NfRRowzQhKeCbKG1hPOE5Zm-RAd34YlVPg-VICDxc0U8MP1_SPFzuNzXwZTOw9Y-xLfQKOLUDmDz1wEHSFuoVWrqwjbn-cmero4fxxfjSZ3l9fj08nIpDlrRjS3nBGjRWlYZq2UJBFac5MUxsoCWK8lOx2qhaRADTe0LCXNNRXcUmKTTXTykbtoizmUBnxT60otajfX9asK2qnfL95N1XNYKikSklHeBex_BtThpYXYqLmLBqpKewhtVCznGeFSkB7d-4POQlv7br2eIiKlJGEdtfvT6Fvl6187gHwApg4x1mCVcY1uXOgFXaUoUX11qq9OvVfXjRz8GflK_Qd-AyORmGM
CitedBy_id crossref_primary_10_3389_fendo_2023_1219194
crossref_primary_10_1186_s12951_025_03401_2
crossref_primary_10_1016_j_scispo_2025_08_003
crossref_primary_10_1016_j_tem_2025_05_005
crossref_primary_10_1007_s10735_025_10460_0
crossref_primary_10_1016_j_biopha_2024_117176
crossref_primary_10_3390_app142412051
crossref_primary_10_1002_cbic_202400883
crossref_primary_10_1002_mco2_70135
crossref_primary_10_1016_j_intimp_2024_112201
crossref_primary_10_1007_s11033_024_09406_8
crossref_primary_10_1016_j_freeradbiomed_2025_05_400
crossref_primary_10_1016_j_taap_2025_117560
crossref_primary_10_1186_s13287_025_04579_w
crossref_primary_10_2147_JPR_S517711
crossref_primary_10_3390_ijms25052600
crossref_primary_10_1016_j_phymed_2023_155132
crossref_primary_10_1038_s41598_023_50084_6
crossref_primary_10_1007_s11010_025_05297_w
crossref_primary_10_1007_s13577_025_01285_w
crossref_primary_10_1111_jcmm_70605
crossref_primary_10_1016_j_rvsc_2024_105177
crossref_primary_10_3389_fcell_2025_1525294
crossref_primary_10_3390_cells14141113
crossref_primary_10_3390_nu16081166
crossref_primary_10_1186_s40001_025_02862_3
crossref_primary_10_1016_j_cdnut_2025_107548
crossref_primary_10_1016_j_biopha_2023_116110
crossref_primary_10_1007_s11255_024_04162_x
crossref_primary_10_3390_ijms241914835
crossref_primary_10_1002_slct_202403409
crossref_primary_10_1016_j_jep_2025_120063
crossref_primary_10_1016_j_jep_2025_120386
crossref_primary_10_1089_scd_2023_0204
crossref_primary_10_1177_1934578X251350769
crossref_primary_10_1016_j_cellsig_2024_111478
crossref_primary_10_1016_j_aca_2023_341989
crossref_primary_10_1016_j_freeradbiomed_2024_11_030
crossref_primary_10_1016_j_jnutbio_2024_109604
crossref_primary_10_1016_j_biopha_2025_118367
crossref_primary_10_3390_ijms25094785
crossref_primary_10_1016_j_phymed_2024_156288
crossref_primary_10_1007_s12011_024_04503_y
crossref_primary_10_3892_mmr_2025_13573
crossref_primary_10_1007_s10522_024_10153_3
crossref_primary_10_1016_j_arr_2024_102557
crossref_primary_10_3389_fendo_2025_1553794
crossref_primary_10_1016_j_biopha_2025_118361
crossref_primary_10_1038_s41598_024_67755_7
crossref_primary_10_1038_s41440_024_01991_2
crossref_primary_10_1186_s40795_024_00921_2
crossref_primary_10_3724_abbs_2025039
crossref_primary_10_1007_s12020_024_03823_2
crossref_primary_10_1016_j_biopha_2024_117482
crossref_primary_10_1016_j_phrs_2024_107155
crossref_primary_10_1016_j_intimp_2024_113700
crossref_primary_10_4236_jbm_2025_138006
crossref_primary_10_1016_j_exer_2025_110526
crossref_primary_10_3390_ijms252111488
crossref_primary_10_1038_s41390_024_03747_7
crossref_primary_10_3390_ijms25189788
crossref_primary_10_1016_j_bcp_2024_116554
crossref_primary_10_3389_fendo_2024_1480847
crossref_primary_10_3389_fimmu_2024_1465849
crossref_primary_10_3390_molecules30183740
crossref_primary_10_3390_ijms26052103
crossref_primary_10_1016_j_jare_2025_08_067
crossref_primary_10_1002_mnfr_202400522
crossref_primary_10_3389_fendo_2025_1529231
crossref_primary_10_1007_s12011_025_04828_2
crossref_primary_10_3390_metabo14080418
crossref_primary_10_1016_j_cellsig_2025_111713
crossref_primary_10_3389_fneur_2023_1275266
crossref_primary_10_1016_j_snb_2024_136144
crossref_primary_10_3390_ph18081222
crossref_primary_10_1007_s10854_023_09956_w
ContentType Journal Article
Copyright The author(s).
2023. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
The author(s) 2023
Copyright_xml – notice: The author(s).
– notice: 2023. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: The author(s) 2023
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7QL
7QO
7U9
8FD
8FE
8FG
8FH
ABJCF
ABUWG
AEUYN
AFKRA
AZQEC
BBNVY
BENPR
BGLVJ
BHPHI
C1K
CCPQU
DWQXO
FR3
GNUQQ
H94
HCIFZ
L6V
LK8
M7N
M7P
M7S
P64
PHGZM
PHGZT
PIMPY
PKEHL
PQEST
PQGLB
PQQKQ
PQUKI
PTHSS
RC3
7X8
5PM
DOI 10.7150/ijbs.78654
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Bacteriology Abstracts (Microbiology B)
Biotechnology Research Abstracts
Virology and AIDS Abstracts
Technology Research Database
ProQuest SciTech Collection
ProQuest Technology Collection
ProQuest Natural Science Collection
Materials Science & Engineering Collection
ProQuest Central (Alumni)
ProQuest One Sustainability
ProQuest Central UK/Ireland
ProQuest Central Essentials
Biological Science Collection
ProQuest Central
ProQuest Technology Collection
Natural Science Collection
Environmental Sciences and Pollution Management
ProQuest One
ProQuest Central
Engineering Research Database
ProQuest Central Student
AIDS and Cancer Research Abstracts
SciTech Premium Collection
ProQuest Engineering Collection
Biological Sciences
Algology Mycology and Protozoology Abstracts (Microbiology C)
Biological Science Database
Engineering Database
Biotechnology and BioEngineering Abstracts
ProQuest Central Premium
ProQuest One Academic
ProQuest Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Applied & Life Sciences
ProQuest One Academic (retired)
ProQuest One Academic UKI Edition
Engineering Collection
Genetics Abstracts
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest Central Student
Technology Collection
Technology Research Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Central (Alumni Edition)
SciTech Premium Collection
ProQuest One Community College
ProQuest Natural Science Collection
Environmental Sciences and Pollution Management
ProQuest Central
ProQuest One Applied & Life Sciences
ProQuest One Sustainability
Genetics Abstracts
ProQuest Engineering Collection
Biotechnology Research Abstracts
Natural Science Collection
ProQuest Central Korea
Bacteriology Abstracts (Microbiology B)
Algology Mycology and Protozoology Abstracts (Microbiology C)
Biological Science Collection
AIDS and Cancer Research Abstracts
ProQuest Central (New)
Engineering Collection
Engineering Database
Virology and AIDS Abstracts
ProQuest Biological Science Collection
ProQuest One Academic Eastern Edition
ProQuest Technology Collection
Biological Science Database
ProQuest SciTech Collection
Biotechnology and BioEngineering Abstracts
ProQuest One Academic UKI Edition
Materials Science & Engineering Collection
Engineering Research Database
ProQuest One Academic
ProQuest One Academic (New)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database

MEDLINE - Academic
MEDLINE
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: PIMPY
  name: Publicly Available Content Database
  url: http://search.proquest.com/publiccontent
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 1449-2288
EndPage 501
ExternalDocumentID PMC9830516
36632457
10_7150_ijbs_78654
Genre Research Support, Non-U.S. Gov't
Journal Article
Review
GroupedDBID ---
29J
2WC
4.4
53G
5GY
5VS
AAYXX
ABJCF
ACGFO
ACIWK
ACPRK
ADBBV
ADRAZ
AENEX
AEUYN
AFFHD
AFKRA
AFRAH
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BBNVY
BCNDV
BENPR
BGLVJ
BHPHI
C1A
CCPQU
CITATION
DIK
DU5
E3Z
EBS
EJD
EMOBN
F5P
GROUPED_DOAJ
GX1
HCIFZ
HYE
KQ8
M48
M7P
M7S
M~E
O5R
O5S
OK1
OVT
PGMZT
PHGZM
PHGZT
PIMPY
PQGLB
PTHSS
RNS
RPM
TR2
WOQ
WOW
XSB
CGR
CUY
CVF
ECM
EIF
NPM
7QL
7QO
7U9
8FD
8FE
8FG
8FH
ABUWG
AZQEC
C1K
DWQXO
FR3
GNUQQ
H94
L6V
LK8
M7N
P64
PKEHL
PQEST
PQQKQ
PQUKI
PUEGO
RC3
7X8
5PM
ID FETCH-LOGICAL-c472t-17f620ca8dc25ff99038aa6c3bcf9be2003693241a891e1c6c1dd917a186f10f3
IEDL.DBID M7P
ISICitedReferencesCount 88
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000893586500006&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1449-2288
IngestDate Tue Nov 04 02:06:37 EST 2025
Thu Sep 25 08:53:52 EDT 2025
Sat Sep 06 07:30:25 EDT 2025
Thu Jan 02 22:53:20 EST 2025
Sat Nov 29 06:17:31 EST 2025
Tue Nov 18 22:12:51 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords inhibitors
agonists
SIRT1
endocrine metabolic
Language English
License The author(s).
This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c472t-17f620ca8dc25ff99038aa6c3bcf9be2003693241a891e1c6c1dd917a186f10f3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
These authors contributed equally to this work.
Competing Interests: The authors have declared that no competing interest exists.
OpenAccessLink https://www.proquest.com/docview/2760841032?pq-origsite=%requestingapplication%
PMID 36632457
PQID 2760841032
PQPubID 2046459
PageCount 18
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_9830516
proquest_miscellaneous_2765069806
proquest_journals_2760841032
pubmed_primary_36632457
crossref_citationtrail_10_7150_ijbs_78654
crossref_primary_10_7150_ijbs_78654
PublicationCentury 2000
PublicationDate 2023-00-00
20230101
PublicationDateYYYYMMDD 2023-01-01
PublicationDate_xml – year: 2023
  text: 2023-00-00
PublicationDecade 2020
PublicationPlace Australia
PublicationPlace_xml – name: Australia
– name: Sydney
PublicationTitle International journal of biological sciences
PublicationTitleAlternate Int J Biol Sci
PublicationYear 2023
Publisher Ivyspring International Publisher Pty Ltd
Ivyspring International Publisher
Publisher_xml – name: Ivyspring International Publisher Pty Ltd
– name: Ivyspring International Publisher
SSID ssj0036580
Score 2.605032
SecondaryResourceType review_article
Snippet Silent information regulator 1 (SIRT1), a highly conserved NAD -dependent deacetylase, is a cellular regulator that has received extensive attention in recent...
Silent information regulator 1 (SIRT1), a highly conserved NAD+-dependent deacetylase, is a cellular regulator that has received extensive attention in recent...
SourceID pubmedcentral
proquest
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 484
SubjectTerms Adipocytes
Aging
Apoptosis
Autophagy
Biomarkers
Biomarkers - metabolism
Deacetylation
Diabetes
Diabetes mellitus
Endocrine system
Endocrine System Diseases - diagnosis
Endocrine System Diseases - drug therapy
Endocrine System Diseases - metabolism
Energy metabolism
Female reproductive system
Gene expression
Glucose
Histones
Humans
Hyperlipidemia
Hypertension
Hyperuricemia
Insulin
Kinases
Lipids
Localization
Lysine
Mammals
Melatonin
Metabolic Diseases - diagnosis
Metabolic Diseases - drug therapy
Metabolic Diseases - metabolism
Metabolic disorders
Molecular Targeted Therapy
Osteoporosis
Oxidative stress
Pancreas
Physiology
Polycystic ovary syndrome
Proteins
Review
Senescence
SIRT1 protein
Sirtuin 1 - metabolism
Therapeutic targets
Transcription factors
Transcription Factors - metabolism
Title Novel Role of the SIRT1 in Endocrine and Metabolic Diseases
URI https://www.ncbi.nlm.nih.gov/pubmed/36632457
https://www.proquest.com/docview/2760841032
https://www.proquest.com/docview/2765069806
https://pubmed.ncbi.nlm.nih.gov/PMC9830516
Volume 19
WOSCitedRecordID wos000893586500006&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 1449-2288
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0036580
  issn: 1449-2288
  databaseCode: M~E
  dateStart: 20040101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVPQU
  databaseName: Biological Science Database
  customDbUrl:
  eissn: 1449-2288
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0036580
  issn: 1449-2288
  databaseCode: M7P
  dateStart: 20190101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/biologicalscijournals
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Engineering Database
  customDbUrl:
  eissn: 1449-2288
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0036580
  issn: 1449-2288
  databaseCode: M7S
  dateStart: 20190101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl:
  eissn: 1449-2288
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0036580
  issn: 1449-2288
  databaseCode: BENPR
  dateStart: 20190101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Publicly Available Content Database
  customDbUrl:
  eissn: 1449-2288
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0036580
  issn: 1449-2288
  databaseCode: PIMPY
  dateStart: 20190101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/publiccontent
  providerName: ProQuest
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB71ARIX3o-UsnIFFw6hceKnOCBot6KHrqJtkZZT5PghglZJabaVuPDbayfZLVsQFy6-eBRbM_bM2J58H8AbRTNqNFdxooiLiTQkFlTZWCWOGkdEKanqyCb4ZCJmM5kPF27tUFa59ImdozaNDnfk-ylniSAB_u3D-Y84sEaF19WBQmMTtgNKQtqV7uVLT5z56Jr0kKTc5z371feyfccFo2Q9CP2RWd4ukPwt4hw9-N-5PoT7Q66JPvaL4xFs2Pox3O3ZJ38-gfeT5srO0bSZW9Q45DNBdHo8PcOoqtG49qOEHwORqg06sQu_VuaVRof9e077FL4cjc8OPscDl0KsCU8XMeaOpYlWwuiUOudjUCaUYjortZOlDSVqzKdyBCshscWaaWyMP8opLJjDicuewVbd1PYFICkdl9Rk_iuKSOIUp7SUzuvacO6ziQjeLpVb6AFoPPBdzAt_4AiGKIIhis4QEbxeyZ738Bp_ldpd6rkYtlhb3Cg5gr1Vt98c4cVD1ba57GRowqRIWATPe5OuhslYQKqnPAK-ZuyVQADeXu-pq28dALcU3ktitvPvab2Ee4Gbvr-v2YWtxcWlfQV39NWiai9GsMlnYgTbn8aTfDrq1m3Xnob219j35Mcn-ddrEN_6bg
linkProvider ProQuest
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V3JbtRAEC2FCYhcwg4OARoBBw4mXnoVQgiRRBklMxqFQQon0-5FGI3sJJ4E5af4Rrq9DAwgbjlw7pLd9quuer29AnguSUq0YjKMJLYhFhqHnEgTysgSbTHPBZFNsQk2HvOjIzFZge_9XRh_rLKPiU2g1pXya-RbCaMRx17-7e3xSeirRvnd1b6ERusW--bim5uy1W-G2w7fF0myuzN9vxd2VQVChVkyD2NmaRIpybVKiLUuGqdcSqrSXFmRG39YizpSg2PJRWxiRVWstZvUyJhTG0c2dc-9AqvYO_sAVifD0eRTH_tTl8-jVgSVOaa1VXzN61eMU4KX094fXPb3I5m_5LjdG__b37kJ6x2bRu9a978FK6a8Ddfa-poXd-D1uDo3M3RYzQyqLHJcF30YHk5jVJRop3Rf5a8-IllqNDJzNxpmhULb7Y5VfRc-XkrP78GgrErzAJAQlgmiU_cUiQW2khGSC-uw1Yw5vhTAyx7MTHVS6r6ixyxzUyoPfOaBzxrgA3i2sD1uBUT-arXZ45p1QaTOfoIawNNFsxv-fk9HlqY6a2xIRAWPaAD3WxdavCalXoufsADYknMtDLy0-HJLWXxpJMYFd3kgphv_7tYTuL43HR1kB8Px_kNYSxz_a1enNmEwPz0zj-CqOp8X9enjbpwg-HzZzvcDNedSJg
linkToPdf http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lb9QwEB6VLSAuvB-BAkbAgUPYPPwUQgixXbEqXa1KkcopeB1bBK2S0myL-tf4dYzzWFhA3Hrg7JHtZD7PfLbHMwBPNEtZboQOI01dSFVOQ8m0DXXkWO6onCumm2ITYjqVBwdqtgHf-7cwPqyyt4mNoc4r48_Ih4ngkaQ-_dvQdWERs9H41eHX0FeQ8jetfTmNFiI79vQbbt_ql5MR6vppkoy399-8DbsKA6GhIlmGsXA8iYyWuUmYc2iZU6k1N-ncODW3PnCLI8GhsZYqtrHhJs5z3ODoWHIXRy7Ffs_BJlJymgxgczbZnX3s_UCKvj1qE6IKZF3D4su8fi4kZ3TdBf7Ba38Pz_zF342v_M9_6ipc7lg2ed0ui2uwYcvrcKGtu3l6A15MqxO7IHvVwpLKEeTA5P1kbz8mRUm2S_xC_ySS6DInu3aJq2RRGDJqb7Lqm_DhTGZ-CwZlVdo7QJRyQrE8xV40VdRpwdhcOdRzLgTyqACe9YrNTJdi3Vf6WGS41fIgyDwIsgYEATxeyR62iUX-KrXV6zjrjEud_VRwAI9WzWgW_F2PLm113MiwiCsZ8QBut3BaDZNyn6OfiQDEGtBWAj7l-HpLWXxuUo8rif4h5nf_Pa2HcBERl72bTHfuwaUEaWF7aLUFg-XRsb0P583JsqiPHnRLhsCns8beDx1qWuY
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Novel+Role+of+the+SIRT1+in+Endocrine+and+Metabolic+Diseases&rft.jtitle=International+journal+of+biological+sciences&rft.au=Lu%2C+Chenxi&rft.au=Zhao%2C+Huadong&rft.au=Liu%2C+Yanqing&rft.au=Yang%2C+Zhi&rft.date=2023&rft.eissn=1449-2288&rft.volume=19&rft.issue=2&rft.spage=484&rft_id=info:doi/10.7150%2Fijbs.78654&rft_id=info%3Apmid%2F36632457&rft.externalDocID=36632457
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1449-2288&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1449-2288&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1449-2288&client=summon