About: Are formyl peptide receptors novel targets for therapeutic intervention in ischaemia

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About: Are formyl peptide receptors novel targets for therapeutic intervention in ischaemia–reperfusion injury? 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	Are formyl peptide receptors novel targets for therapeutic intervention in ischaemia–reperfusion injury?
Creator	Gavins, Felicity
Source	Elsevier; Medline; PMC
abstract	Ischaemia–reperfusion (I/R) injury is a common feature of several diseases associated with high morbidity and mortality, such as stroke and myocardial infarction. The damaged tissue displays cardinal signs of inflammation and microvascular injury that, unless resolved, lead to long-term tissue damage with associated dysfunction. Current therapies are limited and are often associated with many side effects. Increasing evidence suggests that members of the formyl peptide receptor (FPR) family, in particular human FPR2/ALX, might have an important role in the pathophysiology of I/R injury. It was recently demonstrated that several peptides and non-peptidyl small-molecule compounds have anti-inflammatory and pro-resolving properties via their action on members of the FPR family. Here I review this evidence and suggest that FPR ligands, particularly in the brain, could be novel and exciting anti-inflammatory therapeutics for the treatment of a variety of clinical conditions, including stroke.
has issue date	2010-05-17(xsd:dateTime)
bibo:doi	10.1016/j.tips.2010.04.001
bibo:pmid	20483490
has license	no-cc
sha1sum (hex)	99ebc69b9e40e9d3736b3c6494bb0911fd635356
schema:url	https://doi.org/10.1016/j.tips.2010.04.001
resource representing a document's title	Are formyl peptide receptors novel targets for therapeutic intervention in ischaemia–reperfusion injury?
has PubMed Central identifier	PMC7112865
has PubMed identifier	20483490
schema:publication	Trends Pharmacol Sci
resource representing a document's body	covid:99ebc69b9e40e9d3736b3c6494bb0911fd635356#body_text
is schema:about of	named entity 'SMALL' named entity 'DEMONSTRATED' named entity 'FPR2' named entity 'TISSUE' named entity 'FPR' named entity 'MEMBERS' named entity 'ISCHAEMIA' named entity 'PRO-' named entity 'LIGANDS' named entity 'INFLAMMATION' named entity 'TREATMENT' named entity 'REVIEW' named entity 'MOLECULE' named entity 'LIMITED' named entity 'SIGNS' named entity 'FEATURE' named entity 'IMPORTANT' named entity 'RESOLVED' named entity 'EVIDENCE' named entity 'INCLUDING' named entity 'FAMILY' named entity 'COULD BE' named entity 'FORMYL PEPTIDE RECEPTOR' named entity 'CURRENT' named entity 'RESOLVING' named entity 'RECENTLY' named entity 'MICROVASCULAR' named entity 'DAMAGED' named entity 'RECEPTORS' named entity 'THEIR' named entity 'A COMMON' named entity 'CARDINAL' named entity 'HUMAN' named entity 'NOVEL' named entity 'ROLE' named entity 'THERAPEUTICS' named entity 'MORBIDITY AND MORTALITY' named entity 'IS A' named entity 'ANTIINFLAMMATORY' named entity 'HERE' named entity 'TARGETS' named entity 'ISCHAEMIA' named entity 'FORMYL' named entity 'THERAPEUTIC INTERVENTION' named entity 'MYOCARDIAL INFARCTION' named entity 'ACTION' named entity 'VARIETY' named entity 'INJURY' named entity 'THE BRAIN' named entity '28I' named entity 'SIDE EFFECTS' named entity 'ANTI-INFLAMMATORY' named entity 'STROKE' named entity 'LONG-TERM' named entity 'PEPTIDES' named entity 'PROPERTIES' named entity 'PARTICULAR' named entity 'CLINICAL' named entity 'HAVE' named entity 'DISEASES' named entity 'PEPTIDE' named entity 'REPERFUSION INJURY' named entity 'NOVEL' named entity 'LEAD' named entity 'REPERFUSION' named entity 'PATHOPHYSIOLOGY' named entity 'CONDITIONS' named entity 'TISSUE DAMAGE' named entity 'THERAPIES' named entity 'DISPLAYS' named entity 'NON-' named entity 'HIGH' named entity 'SUGGEST' named entity 'DYSFUNCTION' named entity 'INCREASING' named entity 'ASSOCIATED WITH' named entity 'PEPTIDYL' named entity 'non-peptide' named entity 'amino acid' named entity 'mitochondrial respiration' named entity 'agonist'

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