About: AT(2) Receptor and Tissue Injury: Therapeutic Implications

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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	AT(2) Receptor and Tissue Injury: Therapeutic Implications
Creator	Editor, Mediators, Mechanisms Pathways In, Tissue Injury (t Fujita, Section
Source	PMC
abstract	The renin-angiotensin system (RAS) plays an important role in the initiation and progression of tissue injuries in the cardiovascular and nervous systems. The detrimental actions of the AT(1) receptor (AT(1)R) in hypertension and vascular injury, myocardial infarction and brain ischemia are well established. In the past twenty years, protective actions of the RAS, not only in the cardiovascular, but also in the nervous system, have been demonstrated. The so-called protective arm of the RAS includes AT(2)-receptors and Mas receptors (AT(2)R and MasR) and is characterized by effects different from and often opposing those of the AT(1)R. These include anti-inflammation, anti-fibrosis, anti-apoptosis and neuroregeneration that can counterbalance pathological processes and enable recovery from disease. The recent development of novel, small-molecule AT(2)R agonists offers a therapeutic potential in humans with a variety of clinical indications.
has issue date	2014-01-11(xsd:dateTime)
bibo:doi	10.1007/s11906-013-0416-6
bibo:pmid	24414230
has license	no-cc
sha1sum (hex)	2748613d79bfec6f3ca800d2862bbde4227a197f
schema:url	https://doi.org/10.1007/s11906-013-0416-6
resource representing a document's title	AT(2) Receptor and Tissue Injury: Therapeutic Implications
has PubMed Central identifier	PMC3906548
has PubMed identifier	24414230
schema:publication	Curr Hypertens Rep
resource representing a document's body	covid:2748613d79bfec6f3ca800d2862bbde4227a197f#body_text
is schema:about of	named entity 'cardiovascular' named entity 'progression' named entity 'demonstrated' named entity 'anti-inflammation' named entity 'RECEPTORS' named entity 'YEARS' named entity 'CARDIOVASCULAR' named entity 'FIBROSIS' named entity 'RAS' named entity 'ACTIONS' named entity 'DISEASE' named entity 'NERVOUS SYSTEM' named entity 'NEUROREGENERATION' named entity 'ROLE' named entity 'INCLUDES' named entity 'VARIETY' named entity 'CLINICAL' named entity 'DIFFERENT' named entity 'INITIATION' named entity 'MasR' named entity 'infarction' named entity 'losartan' named entity 'Alzheimer' named entity 'fat' named entity 'protein phosphatases' named entity 'hypertension' named entity 'dermal fibroblasts' named entity 'receptor' named entity 'protein' named entity 'IL-10' named entity 'BDNF' named entity 'atherosclerosis' named entity 'NADPH oxidase' named entity 'macrophage' named entity 'receptor' named entity 'molecular mechanisms' named entity 'receptor' named entity 'mice' named entity 'knock-out mice' named entity 'receptor' named entity 'oxidative stress' named entity 'cGMP-dependent protein kinase' named entity 'PLZF' named entity 'TrkB' named entity 'cortical neurons' named entity 'neuroprotection' named entity 'NMDA' named entity 'cardiac hypertrophic' named entity 'autocrine' named entity 'spinal cord injury' named entity 'receptor' named entity 'protein kinase' named entity 'Fas' named entity 'neuroprotection' named entity 'Fas' named entity 'receptor' named entity 'receptor' named entity 'extracellular matrix' named entity 'kinase' named entity 'mice' named entity 'hypertension' named entity 'cardiac hypertrophy' named entity 'MMP2' named entity 'TrkB' named entity 'FasL' named entity 'Paulis' named entity 'cardiovascular' named entity 'pathological conditions' named entity 'receptor' named entity 'mitogen-activated protein kinase kinase' named entity 'receptor' named entity 'Ang II' named entity 'receptor' named entity 'MMP2' named entity 'wild-type' named entity 'INF-γ' named entity 'anti-inflammatory' named entity 'apoptotic'

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