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Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease
المؤلفون المشاركون
Rubattu, Speranza
Stanzione, Rosita
Volpe, Massimo
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-08-09
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Mechanisms underlying hypertensive target organ damage (TOD) are not completely understood.
The pathophysiological role of mitochondrial oxidative stress, resulting from mitochondrial dysfunction, in development of TOD is unclear.
The stroke-prone spontaneously hypertensive rat (SHRSP) is a suitable model of human hypertension and of its vascular consequences.
Pathogenesis of TOD in SHRSP is multifactorial, being determined by high blood pressure levels, high salt/low potassium diet, and genetic factors.
Accumulating evidence points to a key role of mitochondrial dysfunction in increased susceptibility to TOD development of SHRSP.
Mitochondrial abnormalities were described in both heart and brain of SHRSP.
Pharmacological compounds able to protect mitochondrial function exerted a significant protective effect on TOD development, independently of blood pressure levels.
Through our research efforts, we discovered that two genes encoding mitochondrial proteins, one (Ndufc2) involved in OXPHOS complex I assembly and activity and the second one (UCP2) involved in clearance of mitochondrial ROS, are responsible, when dysregulated, for vascular damage in SHRSP.
The suitability of SHRSP as a model of human disease represents a promising background for future translation of the experimental findings to human hypertension.
Novel therapeutic strategies toward mitochondrial molecular targets may become a valuable tool for prevention and treatment of TOD in human hypertension.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Rubattu, Speranza& Stanzione, Rosita& Volpe, Massimo. 2016. Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1113589
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Rubattu, Speranza…[et al.]. Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-10.
https://search.emarefa.net/detail/BIM-1113589
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Rubattu, Speranza& Stanzione, Rosita& Volpe, Massimo. Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1113589
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1113589
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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