![](/images/graphics-bg.png)
Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence
المؤلفون المشاركون
Scharffetter-Kochanek, Karin
He, Hong-Peng
Zhang, Yujie
Guo, Peiyan
Xiang, Wanchen
Liu, Qingxi
Liu, Xinyi
Ma, Ning
Zhou, Sa
Wlaschek, Meinhard
Zhang, Tong-Cun
Ma, Wenjian
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-02-10
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Treatments on neoplastic diseases and cancer using genotoxic drugs often cause long-term health problems related to premature aging.
The underlying mechanism is poorly understood.
Based on the study of a long-lasting senescence-like growth arrest (10-12 weeks) of human dermal fibroblasts induced by psoralen plus UVA (PUVA) treatment, we here revealed that slowly repaired bulky DNA damages can serve as a “molecular scar” leading to reduced cell proliferation through persistent endogenous production of reactive oxygen species (ROS) that caused accelerated telomere erosion.
The elevated levels of ROS were the results of mitochondrial dysfunction and the activation of NADPH oxidase (NOX).
A combined inhibition of DNA-PK and PARP1 could suppress the level of ROS.
Together with a reduced expression level of BRCA1 as well as the upregulation of PP2A and 53BP1, these data suggest that the NHEJ repair of DNA double-strand breaks may be the initial trigger of metabolic changes leading to ROS production.
Further study showed that stimulation of the pentose phosphate pathway played an important role for NOX activation, and ROS could be efficiently suppressed by modulating the NADP/NADPH ratio.
Interestingly, feeding cells with ribose-5-phosphate, a precursor for nucleotide biosynthesis that produced through the PPP, could evidently suppress the ROS level and prevent the cell enlargement related to mitochondrial biogenesis.
Taken together, these results revealed an important signaling pathway between DNA damage repair and the cell metabolism, which contributed to the premature aging effects of PUVA, and may be generally applicable for a large category of chemotherapeutic reagents including many cancer drugs.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zhang, Yujie& Guo, Peiyan& Xiang, Wanchen& Liu, Qingxi& Liu, Xinyi& Ma, Ning…[et al.]. 2020. Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204825
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zhang, Yujie…[et al.]. Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1204825
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zhang, Yujie& Guo, Peiyan& Xiang, Wanchen& Liu, Qingxi& Liu, Xinyi& Ma, Ning…[et al.]. Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204825
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204825
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
![](/images/ebook-kashef.png)
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر
![](/images/kashef-image.png)