The Signaling of Cellular Senescence in Diabetic Nephropathy

Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (E...

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Bibliographic Details
Published inOxidative medicine and cellular longevity Vol. 2019; no. 2019; pp. 1 - 16
Main Authors Xiong, Yabing, Zhou, Lili
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 2019
Hindawi
John Wiley & Sons, Inc
Subjects
Aging
Animals
B cells
Cardiovascular diseases
Cell cycle
Cell division
Cellular Senescence
Chronic kidney failure
CRISPR
Cyclin-dependent kinases
Cytokines
Development and progression
Diabetes
Diabetic nephropathies
Diabetic Nephropathies - genetics
Diabetic Nephropathies - metabolism
Diabetic Nephropathies - pathology
Diabetic Nephropathies - therapy
Diabetic nephropathy
DNA Damage
Epigenesis, Genetic
Epigenetic inheritance
Fenofibrate
Glucose
Health aspects
Hemodialysis
Humans
Hyperglycemia
Inflammation
Kidney diseases
Kinases
Medical research
Mitophagy
Nephrology
Oxidative stress
Proteins
Review
Senescence
Signal Transduction
Stem cells
Systematic review
Telomeres
Tumor necrosis factor-TNF
Type 2 diabetes
China
Online AccessGet full text

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Abstract Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/β-catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.
AbstractList Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/β-catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/β-catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.
Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/ β -catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.
Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/β-catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.
Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The patients, commonly complicated with cardiovascular diseases and neurologic disorders, are at high risk to progress into end-stage renal disease (ESRD) and death. However, the pathogenic mechanisms of diabetic nephropathy have not been determined. Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/ -catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies.
Audience Academic
Author Xiong, Yabing
Zhou, Lili
AuthorAffiliation 1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China
2 Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China
AuthorAffiliation_xml – name: 1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China
– name: 2 Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China
Author_xml – sequence: 1
  fullname: Xiong, Yabing
– sequence: 2
  fullname: Zhou, Lili
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31687085$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Copyright © 2019 Yabing Xiong and Lili Zhou.
COPYRIGHT 2019 John Wiley & Sons, Inc.
Copyright © 2019 Yabing Xiong and Lili Zhou. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0
Copyright © 2019 Yabing Xiong and Lili Zhou. 2019
Copyright_xml – notice: Copyright © 2019 Yabing Xiong and Lili Zhou.
– notice: COPYRIGHT 2019 John Wiley & Sons, Inc.
– notice: Copyright © 2019 Yabing Xiong and Lili Zhou. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0
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Snippet Diabetic nephropathy is the leading cause of chronic kidney disease (CKD) in western countries. Notably, it has a rapidly rising prevalence in China. The...
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SubjectTerms Aging
Animals
B cells
Cardiovascular diseases
Cell cycle
Cell division
Cellular Senescence
Chronic kidney failure
CRISPR
Cyclin-dependent kinases
Cytokines
Development and progression
Diabetes
Diabetic nephropathies
Diabetic Nephropathies - genetics
Diabetic Nephropathies - metabolism
Diabetic Nephropathies - pathology
Diabetic Nephropathies - therapy
Diabetic nephropathy
DNA Damage
Epigenesis, Genetic
Epigenetic inheritance
Fenofibrate
Glucose
Health aspects
Hemodialysis
Humans
Hyperglycemia
Inflammation
Kidney diseases
Kinases
Medical research
Mitophagy
Nephrology
Oxidative stress
Proteins
Review
Senescence
Signal Transduction
Stem cells
Systematic review
Telomeres
Tumor necrosis factor-TNF
Type 2 diabetes
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Title The Signaling of Cellular Senescence in Diabetic Nephropathy
URI https://search.emarefa.net/detail/BIM-1205166
https://dx.doi.org/10.1155/2019/7495629
https://www.ncbi.nlm.nih.gov/pubmed/31687085
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https://www.proquest.com/docview/2312278493
https://pubmed.ncbi.nlm.nih.gov/PMC6794967
Volume 2019
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