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Vascular ADAM17 Mediates Organ Damage by Angiotensin II
Satoru , E.; Kwok, H. F.
2016-10-01
AbstractTo further support the role of ADAM17 as a potential therapeutic target for hypertensive end-organ damage, we showed that a human cross-reactive ADAM17 inhibitory monoclonal antibody, A9(B8), prevents vascular remodeling (vascular hypertrophy and perivascular fibrosis) but not hypertension in wild-type mice. Taken together with the reported ADAM17 polymorphism linking to cardiovascular mortality and our past pharmacological study showing epidermal growth factor receptor inhibition prevents angiotensin II–induced cardiovascular remodeling in mice; these preclinical findings strongly suggest that an ADAM17 inhibitor could be a new add-on therapy for hypertensive patients to prevent hypertensive end-organ damage and reduce cardiovascular mortality.
KeywordVascular ADAM17 Angiotensin II ADAM17 inhibitory monoclonal antibody A9(B8)
Language英語English
The Source to ArticlePB_Publication
PUB ID24577
Document TypeReport
CollectionDEPARTMENT OF BIOMEDICAL SCIENCES
Corresponding AuthorSatoru , E.; Kwok, H. F.
Recommended Citation
GB/T 7714
Satoru , E.,Kwok, H. F.. Vascular ADAM17 Mediates Organ Damage by Angiotensin II, 2016.
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