About: ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension
Creator	Lazartigues, Eric Lakkappa, Navya De Queiroz, Thyago
Source	PMC
abstract	The increase of Angiontesin-II (Ang-II), one of the key peptides of the renin-angiotensin system (RAS), and its binding to the Ang-II type 1 receptor (AT(1)R) during hypertension is a crucial mechanism leading to AD/AM17 activation. Among the reported membrane anchored proteins cleaved by ADAM17, immunological cytokines (TNF-α, IFN-γ, TGF-β, IL-4, IL-10, IL-13, IL-6, FKN) are the major class of substrates, modulation of which triggers inflammation. The rise in ADAM17 levels has both central and peripheral implications in inflammation-mediated hypertension. This narrative review provides an overview of the role of ADAM17, with a special focus on its cellular regulation on neuronal and peripheral inflammation-mediated hypertension. Finally, it highlights the importance of ADAM17 with regards to the biology of inflammatory cytokines and their roles in hypertension.
has issue date	2020-07-29(xsd:dateTime)
bibo:doi	10.3389/fphar.2020.01154
has license	cc-by
sha1sum (hex)	0366c66c5b01e20b4c951f0a9b618fb6e70c765e
schema:url	https://doi.org/10.3389/fphar.2020.01154
resource representing a document's title	ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension
has PubMed Central identifier	PMC7403492
schema:publication	Front Pharmacol
resource representing a document's body	covid:0366c66c5b01e20b4c951f0a9b618fb6e70c765e#body_text
is schema:about of	named entity 'focus' named entity 'peripheral' named entity 'RAS' named entity 'type 1' named entity 'levels' named entity 'TGF-b' named entity 'immunological' named entity 'REPORTED' named entity 'LEADING' named entity 'IFN-G' named entity 'ANCHORED' named entity 'PERIPHERAL' named entity 'CLEAVED' named entity 'THEIR' named entity 'PROVIDES' named entity 'OVERVIEW' named entity 'IL-10' named entity 'narrative review' named entity 'ADAM17' named entity 'modulation' named entity 'proteins' named entity 'special' named entity 'neuronal' named entity 'leading' named entity 'peripheral' named entity 'triggers' named entity 'IFN-g' named entity 'Ang-II' named entity 'IL-4' named entity 'Ang-II' named entity 'cellular regulation' named entity 'hypertension' named entity 'ADAM17' named entity 'immunological' named entity 'hypertension' named entity 'ADAM17' named entity 'RAS' named entity 'oxidative stress' named entity 'PVN' named entity 'membrane proteins' named entity 'gp130' named entity 'hypertension' named entity 'IL-1b' named entity 'Ang-II' named entity 'protein' named entity 'kDa' named entity 'endogenous' named entity 'hypertensive nephropathy' named entity 'peptide' named entity 'signaling pathways' named entity 'physiological' named entity 'TNF-a' named entity 'neurons' named entity 'cystein' named entity 'IL-6' named entity 'neuroinflammation' named entity 'blood pressure' named entity 'RAS' named entity 'Ang-II' named entity 'angiotensin converting enzyme' named entity 'TNFa' named entity 'IL-6' named entity 'electrolyte balance' named entity 'hypertension' named entity 'aspartate' named entity 'mice' named entity 'neuroinflammation' named entity 'CXC' named entity 'physiological effects' named entity 'Shang' named entity 'recombinant' named entity 'cell surface' named entity 'IL-6' named entity 'minocycline' named entity 'cytokines' named entity 'vasopressin' named entity 'hypertension' named entity 'receptor' named entity 'ADAM17' named entity 'IL-6R' named entity 'microgliosis'

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