Aging mechanism and treatment progress of Cockayne syndrome
Received:March 21, 2022  
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DOI:10.11915/j.issn.1671-5403.2023.01.013
Key words:Cockayne syndrome  aging  DNA damage  base excision repair  mitochondrial dysfunction This work was supported by the Open Project of National Clinical Research Center for Geriatric Diseases
Author NameAffiliationE-mail
HU Li-Zhu Graduate School,Beijing 100853, China
Faculty of Pediatrics,Beijing 100853, China
Department of Pediatrics, First Medical Center,Beijing 100853, China 
zouliping21@hotmail.comaging 
WANG Jing Faculty of Pediatrics,Beijing 100853, China
Department of Pediatrics, First Medical Center,Beijing 100853, China 
zouliping21@hotmail.comaging 
WANG Qiu-Hong Graduate School,Beijing 100853, China
Faculty of Pediatrics,Beijing 100853, China
Department of Pediatrics, First Medical Center,Beijing 100853, China 
zouliping21@hotmail.comaging 
CHEN Hai-Xu National Clinical Research Center for Geriatric Diseases,Beijing 100853, China
Institute of Geriatrics, Second Medical Center, Chinese PLA General Hospital, Beijing 100853, China 
zouliping21@hotmail.comaging 
ZOU Li-Ping Faculty of Pediatrics,Beijing 100853, China
Department of Pediatrics, First Medical Center,Beijing 100853, China
Beijing Institute for Brain Disorders, Center for Brain Disorders Research of Capital Medical University, Beijing 100069, China 
zouliping21@hotmail.comaging 
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Abstract:
      Cockayne syndrome is a progeria syndrome characterized by skin photosensitivity, growth retardation, visual and auditory loss, degeneration of the nervous system and accelerated aging. In this paper, we introduced the aging manifestations of the syndrome in multi-system organs, reviewed its pathogenic mechanisms of defects in transcription and transcription-coupled nucleotide excision repair, and discussed possible key roles of base excision repair and mitochondrial dysfunction in the pathogenesis. We further elucidated the research progress of targeted therapy for Cockayne syndrome in combination with the researches concerning the pathogenic mechanism of aging.
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