FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2290031963> ?p ?o ?g. }

• W2290031963 endingPage "434" @default.
• W2290031963 startingPage "419" @default.
• W2290031963 abstract "Adenosine is a ubiquitous nucleoside, an integral part of ATP that acts as a homeostatic regulator through the activation of four GPCRs, A1, A2A, A2B, and A3, and through receptor-independent mechanisms. Adenosine levels increase in areas of inflammation and hypoxia, where it protects tissues by restoring the oxygen supply:demand ratio, as well as affecting preconditioning, exerting anti-inflammatory effects, and stimulating angiogenesis. Adenosine favours the resolution of pathologies such as epilepsy, pain, ischaemia, inflammation, and cancer, in which it behaves like a guardian angel against cellular damage. New adenosinergic drugs for pain, inflammatory diseases, and cancer are already in clinical development. The importance of adenosine for human health cannot be overstated. Indeed, this ubiquitous nucleoside is an integral component of ATP, and regulates the function of every tissue and organ in the body. Acting via receptor-dependent and -independent mechanisms [the former mediated via four G-protein-coupled receptors (GPCRs), A1, A2A, A2B, and A3,], it has a significant role in protecting against cell damage in areas of increased tissue metabolism, and combating organ dysfunction in numerous pathological states. Accordingly, raised levels of adenosine have been demonstrated in epilepsy, ischaemia, pain, inflammation, and cancer, in which its behaviour can be likened to that of a guardian angel, even though there are instances in which overproduction of adenosine is pathological. In this review, we condense the current body of knowledge on the issue, highlighting when, where, and how adenosine exerts its protective effects in both the brain and the periphery. The importance of adenosine for human health cannot be overstated. Indeed, this ubiquitous nucleoside is an integral component of ATP, and regulates the function of every tissue and organ in the body. Acting via receptor-dependent and -independent mechanisms [the former mediated via four G-protein-coupled receptors (GPCRs), A1, A2A, A2B, and A3,], it has a significant role in protecting against cell damage in areas of increased tissue metabolism, and combating organ dysfunction in numerous pathological states. Accordingly, raised levels of adenosine have been demonstrated in epilepsy, ischaemia, pain, inflammation, and cancer, in which its behaviour can be likened to that of a guardian angel, even though there are instances in which overproduction of adenosine is pathological. In this review, we condense the current body of knowledge on the issue, highlighting when, where, and how adenosine exerts its protective effects in both the brain and the periphery. defined as pain that lasts longer than 12 weeks. pain associated with tissue injury and inflammation, autoimmune disease, or exposure to irritating agents. a process where repeated short, sublethal insults protect the tissue against subsequent ischaemic damage. pain induced by injury or damage that concerns the sensory system. pain caused by ongoing noxious stimuli, such as heat, cold, and chemicals, or acute injury. cell with a single nucleus that synthesises bone. a large multinucleate cell that is closely associated with areas of bone resorption. the tissue damage caused when blood supply returns to the tissue after a period of ischaemia or lack of oxygen (anoxia or hypoxia)." @default.
• W2290031963 created "2016-06-24" @default.
• W2290031963 creator A5013716423 @default.
• W2290031963 creator A5018360276 @default.
• W2290031963 creator A5020435407 @default.
• W2290031963 creator A5027485003 @default.
• W2290031963 date "2016-06-01" @default.
• W2290031963 modified "2023-10-16" @default.
• W2290031963 title "Adenosine as a Multi-Signalling Guardian Angel in Human Diseases: When, Where and How Does it Exert its Protective Effects?" @default.
• W2290031963 cites W1065309053 @default.
• W2290031963 cites W1485133278 @default.
• W2290031963 cites W1489725917 @default.
• W2290031963 cites W1513304310 @default.
• W2290031963 cites W1519097303 @default.
• W2290031963 cites W1575977354 @default.
• W2290031963 cites W1580410057 @default.
• W2290031963 cites W1585020230 @default.
• W2290031963 cites W1594028947 @default.
• W2290031963 cites W1612616533 @default.
• W2290031963 cites W1637996628 @default.
• W2290031963 cites W1778071738 @default.
• W2290031963 cites W1783256508 @default.
• W2290031963 cites W1856034726 @default.
• W2290031963 cites W1891953138 @default.
• W2290031963 cites W1917077661 @default.
• W2290031963 cites W1961839152 @default.
• W2290031963 cites W1965781264 @default.
• W2290031963 cites W1967430693 @default.
• W2290031963 cites W1978362439 @default.
• W2290031963 cites W1982903836 @default.
• W2290031963 cites W1986988959 @default.
• W2290031963 cites W1988427233 @default.
• W2290031963 cites W1990113288 @default.
• W2290031963 cites W1990562629 @default.
• W2290031963 cites W1992267258 @default.
• W2290031963 cites W1994703283 @default.
• W2290031963 cites W1995475470 @default.
• W2290031963 cites W1995858393 @default.
• W2290031963 cites W1997324590 @default.
• W2290031963 cites W1998752508 @default.
• W2290031963 cites W2005911006 @default.
• W2290031963 cites W2008299531 @default.
• W2290031963 cites W2012189513 @default.
• W2290031963 cites W2013927247 @default.
• W2290031963 cites W2016069947 @default.
• W2290031963 cites W2016793143 @default.
• W2290031963 cites W2017930365 @default.
• W2290031963 cites W2020196989 @default.
• W2290031963 cites W2021533537 @default.
• W2290031963 cites W2022159206 @default.
• W2290031963 cites W2028337965 @default.
• W2290031963 cites W2029845823 @default.
• W2290031963 cites W2032169621 @default.
• W2290031963 cites W2032609258 @default.
• W2290031963 cites W2033359295 @default.
• W2290031963 cites W2035369520 @default.
• W2290031963 cites W2035516924 @default.
• W2290031963 cites W2037707394 @default.
• W2290031963 cites W2040716650 @default.
• W2290031963 cites W2043667693 @default.
• W2290031963 cites W2047908801 @default.
• W2290031963 cites W2049194594 @default.
• W2290031963 cites W2049447530 @default.
• W2290031963 cites W2050817125 @default.
• W2290031963 cites W2054262436 @default.
• W2290031963 cites W2057213084 @default.
• W2290031963 cites W2058014722 @default.
• W2290031963 cites W2059079363 @default.
• W2290031963 cites W2061858371 @default.
• W2290031963 cites W2063407553 @default.
• W2290031963 cites W2064342455 @default.
• W2290031963 cites W2067846325 @default.
• W2290031963 cites W2069423981 @default.
• W2290031963 cites W2069507921 @default.
• W2290031963 cites W2071678082 @default.
• W2290031963 cites W2075889121 @default.
• W2290031963 cites W2076590867 @default.
• W2290031963 cites W2077355368 @default.
• W2290031963 cites W2081626751 @default.
• W2290031963 cites W2083496369 @default.
• W2290031963 cites W2086437277 @default.
• W2290031963 cites W2087838893 @default.
• W2290031963 cites W2091815611 @default.
• W2290031963 cites W2093091120 @default.
• W2290031963 cites W2093924523 @default.
• W2290031963 cites W2098566314 @default.
• W2290031963 cites W2099143798 @default.
• W2290031963 cites W2099292201 @default.
• W2290031963 cites W2100363461 @default.
• W2290031963 cites W2104024807 @default.
• W2290031963 cites W2104483410 @default.
• W2290031963 cites W2104599451 @default.
• W2290031963 cites W2107207706 @default.
• W2290031963 cites W2110418038 @default.
• W2290031963 cites W2111788554 @default.
• W2290031963 cites W2114091414 @default.
• W2290031963 cites W2116532890 @default.
• W2290031963 cites W2116863239 @default.

• next