Renal Fibrosis: SIRT1 Still of Value

Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibr...

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Published inBiomedicines Vol. 12; no. 9; p. 1942
Main Authors Wu, Huailiang, Qiu, Zhen, Wang, Liyan, Li, Wei
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.09.2024
MDPI
Subjects
Adenosine
Aging
Amino acids
Apoptosis
Autophagy
Cell cycle
Development and progression
DNA methylation
End-stage renal disease
Energy
Extracellular matrix
Fatty acids
Fibroblasts
Fibrosis
Health aspects
Histones
Homeostasis
Inflammation
Kidney diseases
Lipid metabolism
Metabolism
Metabolites
NAD
Oxidation
Oxidative metabolism
Oxidative stress
Physiological aspects
Physiology
Proteins
Public health
renal fibrosis
Review
Ribosomal DNA
SIRT1
SIRT1 protein
Stem cells
Therapeutic targets
Transcription factors
Trimetazidine
China
aging
renal fibrosis
SIRT1
oxidative stress
lipid metabolism
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Abstract Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
AbstractList Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD )-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD[sup.+])-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to end-stage renal disease. Glomerulosclerosis and renal interstitial fibrosis are the primary pathological features. Preventing and slowing renal fibrosis are considered effective strategies for delaying CKD progression. However, effective treatments are lacking. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD + )-dependent deacetylase belonging to class III histone deacetylases, is implicated in the physiological regulation and protection of the kidney and is susceptible to a diverse array of pathological influences, as demonstrated in previous studies. Interestingly, controversial conclusions have emerged as research has progressed. This review provides a comprehensive summary of the current understanding and advancements in the field; specifically, the biological roles and mechanisms of SIRT1 in regulating renal fibrosis progression. These include aspects such as lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy. This manuscript explores the potential of SIRT1 as a therapeutic target for renal fibrosis and offers new perspectives on treatment approaches and prognostic assessments.
Audience Academic
Author Li, Wei
Wang, Liyan
Qiu, Zhen
Wu, Huailiang
AuthorAffiliation 2 Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan 430060, China; wlyan360@163.com
1 Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; whliang360@163.com (H.W.); qiuzhen124@126.com (Z.Q.)
AuthorAffiliation_xml – name: 1 Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; whliang360@163.com (H.W.); qiuzhen124@126.com (Z.Q.)
– name: 2 Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan 430060, China; wlyan360@163.com
Author_xml – sequence: 1
  givenname: Huailiang
  surname: Wu
  fullname: Wu, Huailiang
– sequence: 2
  givenname: Zhen
  surname: Qiu
  fullname: Qiu, Zhen
– sequence: 3
  givenname: Liyan
  surname: Wang
  fullname: Wang, Liyan
– sequence: 4
  givenname: Wei
  surname: Li
  fullname: Li, Wei
BackLink https://www.ncbi.nlm.nih.gov/pubmed/39335456$$D View this record in MEDLINE/PubMed
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CitedBy_id crossref_primary_10_1186_s10020_025_01071_2
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Keywords aging
renal fibrosis
SIRT1
oxidative stress
lipid metabolism
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Snippet Chronic kidney disease (CKD) is a major global health concern. Renal fibrosis, a prevalent outcome regardless of the initial cause, ultimately leads to...
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SubjectTerms Adenosine
Aging
Amino acids
Apoptosis
Autophagy
Cell cycle
Development and progression
DNA methylation
End-stage renal disease
Energy
Extracellular matrix
Fatty acids
Fibroblasts
Fibrosis
Health aspects
Histones
Homeostasis
Inflammation
Kidney diseases
Lipid metabolism
Metabolism
Metabolites
NAD
Oxidation
Oxidative metabolism
Oxidative stress
Physiological aspects
Physiology
Proteins
Public health
renal fibrosis
Review
Ribosomal DNA
SIRT1
SIRT1 protein
Stem cells
Therapeutic targets
Transcription factors
Trimetazidine
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Title Renal Fibrosis: SIRT1 Still of Value
URI https://www.ncbi.nlm.nih.gov/pubmed/39335456
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Volume 12
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