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Autophagy in homocysteine­induced HUVEC senescence.
Zhang, Yexi; Ouyang, Juyan; Zhan, Liu; Li, Yu; Li, Shaoshan; He, Yi; Wang, Hong; Zhang, Xiangyang.
Afiliación
  • Zhang Y; Department of Functional Examination, Northern Jiangsu People's Hospital, The Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu 225000, P.R. China.
  • Ouyang J; Department of Geriatrics, The First Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang Uyghur Autonomous Region 830000, P.R. China.
  • Zhan L; Department of Functional Science, Karamay College of Xinjiang Medical University, Karamay, Xinjiang Uyghur Autonomous Region 834000, P.R. China.
  • Li Y; Department of Geriatrics, The First Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang Uyghur Autonomous Region 830000, P.R. China.
  • Li S; Department of Clinical Teaching, Karamay College of Xinjiang Medical University, Karamay, Xinjiang Uyghur Autonomous Region 834000, P.R. China.
  • He Y; Department of Morphology, Karamay College of Xinjiang Medical University, Karamay, Xinjiang Uyghur Autonomous Region 834000, P.R. China.
  • Wang H; Department of Geriatrics, The First Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang Uyghur Autonomous Region 830000, P.R. China.
  • Zhang X; Department of Cardiology, The First Affiliated Hospital of Xinjiang Medical University, Urumchi, Xinjiang Uyghur Autonomous Region 830000, P.R. China.
Exp Ther Med ; 26(1): 354, 2023 Jul.
Article en En | MEDLINE | ID: mdl-37324509
The senescence of vascular endothelial cells (VECs) drives the occurrence and development of cardiovascular disease (CVD). Homocysteine (HCY) is a general risk factor for age-associated CVDs. Autophagy, an evolutionarily conserved lysosomal protein degradation pathway, serves a part in VEC senescence. The purpose of this study was to investigate the role of autophagy in HCY-induced endothelial cell senescence and explore novel mechanisms and therapeutic approaches for related CVDs. Human umbilical vein endothelial cells (HUVECs) were isolated from fresh umbilical cords of healthy pregnancies. Cell Counting Kit-8, flow cytometry and senescence-associated (SA) ß-galactosidase (Gal) staining demonstrated that HCY induced HUVEC senescence by decreasing cell proliferation, arresting cell cycle and increasing the number of SA-ß-Gal-positive cells. Stub-RFP-Sens-GFP-LC3 autophagy-related double fluorescence lentivirus revealed that HCY increased autophagic flux. Further, inhibition of autophagy using 3-methyladenine increased HCY-induced HUVEC senescence. By contrast, the induction of autophagy via rapamycin alleviated HCY-induced HUVEC senescence. Finally, the detection of reactive oxygen species (ROS) with ROS kit showed that HCY increased intracellular ROS, whereas induction of autophagy reduced intracellular ROS. In conclusion, HCY increased HUVEC senescence and upregulated autophagy; moderate autophagy could reverse HCY-induced cell senescence. Autophagy may alleviate HCY-induced cell senescence by decreasing intracellular ROS. This provides insight into the underlying mechanism of HCY-induced VEC senescence and potential treatments for age-associated CVDs.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Risk_factors_studies Idioma: En Revista: Exp Ther Med Año: 2023 Tipo del documento: Article Pais de publicación: Grecia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Risk_factors_studies Idioma: En Revista: Exp Ther Med Año: 2023 Tipo del documento: Article Pais de publicación: Grecia