About: ACE2-Ang-(1-7)-Mas Axis in Brain: A Potential Target for Prevention and Treatment of Ischemic Stroke

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About: ACE2-Ang-(1-7)-Mas Axis in Brain: A Potential Target for Prevention and Treatment of Ischemic Stroke Goto Sponge NotDistinct Permalink

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	ACE2-Ang-(1-7)-Mas Axis in Brain: A Potential Target for Prevention and Treatment of Ischemic Stroke
Creator	Gao, Li Jiang, Teng Lu, Jie Zhang, Ying-Dong
topic	covid:6fe01cb9f2b36418bd0f5a17bc665e2e02fd2460#this
Source	PMC
abstract	The renin-angiotensin system (RAS) in brain is a crucial regulator for physiological homeostasis and diseases of cerebrovascular system, such as ischemic stroke. Overactivation of brain Angiotensin-converting enzyme (ACE) - Angiotensin II (Ang II) - Angiotensin II type 1 receptor (AT(1)R) axis was found to be involved in the progress of hypertension, atherosclerosis and thrombogenesis, which increased the susceptibility to ischemic stroke. Besides, brain Ang II levels have been revealed to be increased in ischemic tissues after stroke, and contribute to neural damage through elevating oxidative stress levels and inducing inflammatory response in the ischemic hemisphere via AT(1)R. In recent years, new components of RAS have been discovered, including ACE2, Angiotensin-(1–7) [Ang-(1-7)] and Mas, which constitute ACE2-Ang-(1-7)-Mas axis. ACE2 converts Ang II to Ang-(1-7), and Ang-(1-7) binds with its receptor Mas, exerting benefical effects in cerebrovascular disease. Through interacting with nitric oxide and bradykinin, Ang-(1-7) could attenuate the development of hypertension and the pathologic progress of atherosclerosis. Besides, its antithrombotic activity also prevents thrombogenic events, which may contribute to reduce the risk of ischemic stroke. In addition, after ischemia insult, ACE2-Ang-(1-7)-Mas has been shown to reduce the cerebral infarct size and improve neurological deficits through its antioxidative and anti-inflammatory effects. Taken together, activation of the ACE2-Ang-(1-7)-Mas axis may become a novel therapeutic target in prevention and treatment of ischemia stroke, which deserves further investigations.
has issue date	2013-03-01(xsd:dateTime)
bibo:doi	10.2174/1570159x11311020007
bibo:pmid	23997755
has license	cc-by
sha1sum (hex)	6fe01cb9f2b36418bd0f5a17bc665e2e02fd2460
schema:url	https://doi.org/10.2174/1570159x11311020007
resource representing a document's title	ACE2-Ang-(1-7)-Mas Axis in Brain: A Potential Target for Prevention and Treatment of Ischemic Stroke
has PubMed Central identifier	PMC3637674
has PubMed identifier	23997755
schema:publication	Curr Neuropharmacol
resource representing a document's body	covid:6fe01cb9f2b36418bd0f5a17bc665e2e02fd2460#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/6fe01cb9f2b36418bd0f5a17bc665e2e02fd2460
is schema:about of	named entity 'ACE2' named entity 'TARGET' named entity 'PREVENTION' named entity 'ORDERS' named entity 'cerebrovascular' named entity 'elevating' named entity 'Orders' named entity 'Treatment' named entity 'Target' named entity 'Send' named entity 'ANG' named entity 'RECEPTOR' named entity 'INVOLVED' named entity 'ANGIOTENSIN II' named entity 'NEURAL DAMAGE' named entity 'PROGRESS' named entity 'AXIS' named entity 'PHYSIOLOGICAL HOMEOSTASIS' named entity 'ISCHEMIC' named entity 'ISCHEMIC STROKE' named entity 'INDUCING' named entity 'STROKE' named entity 'CONTRIBUTE ' named entity 'LEVELS' named entity 'MAS' named entity 'SUSCEPTIBILITY TO ISCHEMIC STROKE' named entity 'BRAIN' named entity 'AXIS' named entity 'TREATMENT OF ISCHEMIC STROKE' named entity 'NET' named entity 'SEND' named entity 'POTENTIAL' named entity 'HYPERTENSION' named entity 'ANGIOTENSIN-CONVERTING ENZYME' named entity 'II TYPE' named entity 'HEMISPHERE' named entity 'FOUND' named entity 'IS A' named entity 'ELEVATING' named entity 'DISEASES' named entity 'OXIDATIVE STRESS' named entity 'ATHEROSCLEROSIS' named entity 'REGULATOR' named entity 'TYPE 1' named entity 'TISSUES' named entity 'HAVE' named entity 'REVEALED' named entity 'CEREBROVASCULAR SYSTEM' named entity 'INCREASED' named entity 'INFLAMMATORY RESPONSE' named entity 'RENIN-ANGIOTENSIN SYSTEM' named entity 'BRAIN' named entity 'type 1' named entity 'ischemic' named entity 'inflammatory response' named entity 'levels' named entity 'susceptibility' named entity 'hypertension' named entity 'thrombogenesis' named entity 'inflammatory response' named entity 'renin-angiotensin' named entity 'receptor' named entity 'ischemic' named entity 'ischemic stroke' named entity 'receptor' named entity 'receptor' named entity 'cerebrovascular' named entity 'RAS' named entity '1-7' named entity 'ischemic stroke' named entity 'antithrombotic' named entity 'neurons' named entity 'cerebral blood flow' named entity 'reactive oxygen species' named entity 'ischemia' named entity 'RAS'

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