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Article: Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery
Title | Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery |
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Authors | |
Keywords | caveolin-1 Ischemic stroke MMPs natural compound reactive nitrogen species (RNS) |
Issue Date | 2018 |
Publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html |
Citation | Acta Pharmacologica Sinica, 2018, v. 39, p. 669-682 How to Cite? |
Abstract | Reactive nitrogen species (RNS) play important roles in mediating cerebral ischemia-reperfusion injury. RNS activate multiple signaling pathways and participate in different cellular events in cerebral ischemia-reperfusion injury. Recent studies have indicated that caveolin-1 and matrix metalloproteinase (MMP) are important signaling molecules in the pathological process of ischemic brain injury. During cerebral ischemia-reperfusion, the production of nitric oxide (NO) and peroxynitrite (ONOO-), two representative RNS, down-regulates the expression of caveolin-1 (Cav-1) and, in turn, further activates nitric oxide synthase (NOS) to promote RNS generation. The increased RNS further induce MMP activation and mediate disruption of the blood-brain barrier (BBB), aggravating the brain damage in cerebral ischemia-reperfusion injury. Therefore, the feedback interaction among RNS/Cav-1/MMPs provides an amplified mechanism for aggravating ischemic brain damage during cerebral ischemia-reperfusion injury. Targeting the RNS/Cav-1/MMP pathway could be a promising therapeutic strategy for protecting against cerebral ischemia-reperfusion injury. In this mini-review article, we highlight the important role of the RNS/Cav-1/MMP signaling cascades in ischemic stroke injury and review the current progress of studies seeking therapeutic compounds targeting the RNS/Cav-1/MMP signaling cascades to attenuate cerebral ischemia-reperfusion injury. Several representative natural compounds, including calycosin-7-O-β-D-glucoside, baicalin, Momordica charantia polysaccharide (MCP), chlorogenic acid, lutein and lycopene, have shown potential for targeting the RNS/Cav-1/MMP signaling pathway to protect the brain in ischemic stroke. Therefore, the RNS/Cav-1/MMP pathway is an important therapeutic target in ischemic stroke treatment. |
Persistent Identifier | http://hdl.handle.net/10722/252130 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 1.882 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Chen, H | - |
dc.contributor.author | Chen, X | - |
dc.contributor.author | LI, W | - |
dc.contributor.author | Shen, J | - |
dc.date.accessioned | 2018-04-11T02:26:59Z | - |
dc.date.available | 2018-04-11T02:26:59Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Acta Pharmacologica Sinica, 2018, v. 39, p. 669-682 | - |
dc.identifier.issn | 1671-4083 | - |
dc.identifier.uri | http://hdl.handle.net/10722/252130 | - |
dc.description.abstract | Reactive nitrogen species (RNS) play important roles in mediating cerebral ischemia-reperfusion injury. RNS activate multiple signaling pathways and participate in different cellular events in cerebral ischemia-reperfusion injury. Recent studies have indicated that caveolin-1 and matrix metalloproteinase (MMP) are important signaling molecules in the pathological process of ischemic brain injury. During cerebral ischemia-reperfusion, the production of nitric oxide (NO) and peroxynitrite (ONOO-), two representative RNS, down-regulates the expression of caveolin-1 (Cav-1) and, in turn, further activates nitric oxide synthase (NOS) to promote RNS generation. The increased RNS further induce MMP activation and mediate disruption of the blood-brain barrier (BBB), aggravating the brain damage in cerebral ischemia-reperfusion injury. Therefore, the feedback interaction among RNS/Cav-1/MMPs provides an amplified mechanism for aggravating ischemic brain damage during cerebral ischemia-reperfusion injury. Targeting the RNS/Cav-1/MMP pathway could be a promising therapeutic strategy for protecting against cerebral ischemia-reperfusion injury. In this mini-review article, we highlight the important role of the RNS/Cav-1/MMP signaling cascades in ischemic stroke injury and review the current progress of studies seeking therapeutic compounds targeting the RNS/Cav-1/MMP signaling cascades to attenuate cerebral ischemia-reperfusion injury. Several representative natural compounds, including calycosin-7-O-β-D-glucoside, baicalin, Momordica charantia polysaccharide (MCP), chlorogenic acid, lutein and lycopene, have shown potential for targeting the RNS/Cav-1/MMP signaling pathway to protect the brain in ischemic stroke. Therefore, the RNS/Cav-1/MMP pathway is an important therapeutic target in ischemic stroke treatment. | - |
dc.language | eng | - |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html | - |
dc.relation.ispartof | Acta Pharmacologica Sinica | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | caveolin-1 | - |
dc.subject | Ischemic stroke | - |
dc.subject | MMPs | - |
dc.subject | natural compound | - |
dc.subject | reactive nitrogen species (RNS) | - |
dc.title | Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery | - |
dc.type | Article | - |
dc.identifier.email | Chen, H: chenhs@hku.hk | - |
dc.identifier.email | Shen, J: shenjg@hku.hk | - |
dc.identifier.authority | Shen, J=rp00487 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1038/aps.2018.27 | - |
dc.identifier.scopus | eid_2-s2.0-85046637548 | - |
dc.identifier.hkuros | 284800 | - |
dc.identifier.volume | 39 | - |
dc.identifier.spage | 669 | - |
dc.identifier.epage | 682 | - |
dc.identifier.isi | WOS:000431513300003 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 1671-4083 | - |