Your browser doesn't support javascript.
loading
Loss of Cisd2 Exacerbates the Progression of Age-Related Hearing Loss.
Chen, Hang-Kang; Wang, Yen-Hsin; Lei, Cing-Syuan; Guo, Yu-Ru; Tang, Ming-Chi; Tsai, Ting-Fen; Chen, Yi-Fan; Wang, Chih-Hung.
Afiliación
  • Chen HK; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114201, Taiwan.
  • Wang YH; Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei 114201, Taiwan.
  • Lei CS; Department of Otolaryngology-Head and Neck Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114202, Taiwan.
  • Guo YR; The Ph.D. Program for Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan.
  • Tang MC; Ph.D. Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei 11031, Taiwan.
  • Tsai TF; The Ph.D. Program for Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan.
  • Chen YF; The Ph.D. Program for Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan.
  • Wang CH; Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 11221, Taiwan.
Aging Dis ; 2024 Aug 30.
Article en En | MEDLINE | ID: mdl-39226169
ABSTRACT
Age-related hearing loss (ARHL) is a disease that impacts human quality of life and contributes to the progression of other neuronal problems. Various stressors induce an increase in free radicals, destroy mitochondria to further contribute to cellular malfunction, and compromise cell viability, ultimately leading to functional decline. Cisd2, a master gene for Marfan syndrome, plays an essential role in maintaining mitochondrial integrity and functions. As shown by our data, specific deletion of Cisd2 in the cochlea exacerbated the hearing impairment of ARHL in C57BL/6 mice. Increased defects in mitochondrial function, potassium homeostasis and synapse activity were observed in the Cisd2-deleted mouse models. These mechanistic phenotypes combined with oxidative stress contribute to cell death in the whole cochlea. Human patients with obviously deteriorated ARHL had low Cisd2 expression; therefore, Cisd2 may be a potential target for designing therapeutic methods to attenuate the disease progression of ARHL.
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Aging Dis Año: 2024 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Aging Dis Año: 2024 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos