کد مقاله کد نشریه سال انتشار مقاله انگلیسی ترجمه فارسی نسخه تمام متن
5534602 1551268 2017 8 صفحه PDF سفارش دهید دانلود رایگان
عنوان انگلیسی مقاله ISI
Disruption of transforming growth factor-β superfamily signaling: A shared mechanism underlying hereditary cerebral small vessel disease
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موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Disruption of transforming growth factor-β superfamily signaling: A shared mechanism underlying hereditary cerebral small vessel disease
چکیده انگلیسی


- Molecular pathogenesis of hereditary cerebral small vessel disease.
- Involvement of TGF-β superfamily in hereditary cerebral small vessel disease.
- Future treatment strategy of small vessel disease by targeting TGF-β superfamily.

Cerebral small vessel disease (SVD) is not only one of the leading causes of cognitive impairment but also an important contributory factor in Alzheimer's disease. SVD and related white matter changes are common in the elderly, but the underlying pathogenic mechanism remains unclear. The end-stage pathology of SVD often involves replacement of vascular smooth muscle cells with collagenous or other nontensile fibrillary material. Recent studies on hereditary SVD have revealed a close relationship between small vessel pathology and disruption of transforming growth factor-β (TGF-β) superfamily signaling. TGF-β superfamily members, such as TGF-β and bone morphogenetic proteins, are multifunctional proteins that regulate production of extracellular matrix proteins, which in turn control the bioavailability of TGF-β superfamily members and modulate their signaling activities. This article reviews hereditary disorders with small vessel pathology and their relation to TGF-β superfamily signaling.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 107, July 2017, Pages 211-218
نویسندگان
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