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Hypoxia and Inflammation as a Consequence of β-Fibril Accumulation: A Perspective View for New Potential Therapeutic Targets
المؤلفون المشاركون
Russo, M. A.
Sansone, Luigi
Vernucci, Enza
Tomino, Carlo
Tafani, Marco
Limana, Federica
Frustaci, Andrea
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-06-26
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Amyloidoses are heterogeneous diseases that result from the deposition of toxic insoluble β-sheet fibrillar protein aggregates in different tissues.
The cascade of molecular events leading to amyloidoses and to the related clinical manifestations is not completely understood.
Nevertheless, it is known that tissue damage associated to this disease involves alteration of tissue architecture, interaction with cell surface receptors, inflammation elicited by the amyloid protein deposition, oxidative stress, and apoptosis.
However, another important aspect to consider is that systemic protein massive deposition not only subverts tissue architecture but also determines a progressive cellular hypertrophy and dilation of the extracellular space enlarging the volume of the organ.
Such an alteration increases the distance between cells and vessels with a drop in pO2 that, in turn, causes both necrotic cell death and activation of the hypoxia transcription factor HIF-1α.
Herewith, we propose the hypothesis that both cell death and hypoxia represent two important events for the pathogenesis of damage and progression of amyloidoses.
In fact, molecules released by necrotic cells activate inflammatory cells from one side while binding to HIF-1α-dependent membrane receptors expressed on hypoxic parenchymal cells on the other side.
This latter event generates a signaling cascade triggering NFκB activation and chronic inflammation.
Finally, we also suggest that this scenario, once proved and detailed, might suggest important targets for new therapeutic interventions.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Russo, M. A.& Tomino, Carlo& Vernucci, Enza& Limana, Federica& Sansone, Luigi& Frustaci, Andrea…[et al.]. 2019. Hypoxia and Inflammation as a Consequence of β-Fibril Accumulation: A Perspective View for New Potential Therapeutic Targets. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205353
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Russo, M. A.…[et al.]. Hypoxia and Inflammation as a Consequence of β-Fibril Accumulation: A Perspective View for New Potential Therapeutic Targets. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-10.
https://search.emarefa.net/detail/BIM-1205353
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Russo, M. A.& Tomino, Carlo& Vernucci, Enza& Limana, Federica& Sansone, Luigi& Frustaci, Andrea…[et al.]. Hypoxia and Inflammation as a Consequence of β-Fibril Accumulation: A Perspective View for New Potential Therapeutic Targets. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205353
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1205353
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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