The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia
Stroke is one of the major causes of mortality and morbidity worldwide, yet novel therapeutic treatments for this condition are lacking. This review focuses on the roles of the transient receptor potential melastatin 2 (TRPM2) ion channels in cellular damage following hypoxia-ischemia and their pote...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2018-05, Vol.39 (5), p.713-721 |
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| creator | Turlova, Ekaterina Feng, Zhong-ping Sun, Hong-shuo |
| description | Stroke is one of the major causes of mortality and morbidity worldwide, yet novel therapeutic treatments for this condition are lacking. This review focuses on the roles of the transient receptor potential melastatin 2 (TRPM2) ion channels in cellular damage following hypoxia-ischemia and their potential as a future therapeutic target for stroke. Here, we highlight the complex molecular signaling that takes place in neurons, glial cells and the blood-brain barrier following ischemic insult. We also describe the evidence of TRPM2 involvement in these processes, as shown from numerous
in vitro
and
in vivo
studies that utilize genetic and pharmacological approaches. This evidence implicates TRPM2 in a broad range of pathways that take place every stage of cerebral ischemic injury, thus making TRPM2 a promising target for drug development for stroke and other neurodegenerative conditions of the central nervous system. |
| doi_str_mv | 10.1038/aps.2017.194 |
| format | Article |
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in vitro
and
in vivo
studies that utilize genetic and pharmacological approaches. This evidence implicates TRPM2 in a broad range of pathways that take place every stage of cerebral ischemic injury, thus making TRPM2 a promising target for drug development for stroke and other neurodegenerative conditions of the central nervous system.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2017.194</identifier><identifier>PMID: 29542681</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Blood-brain barrier ; Brain injury ; Central nervous system ; Drug development ; Glial cells ; Hypoxia ; Immunology ; Internal Medicine ; Ion channels ; Ischemia ; Medical Microbiology ; Molecular chains ; Morbidity ; Neuronal-glial interactions ; Neurons ; Pharmacology/Toxicology ; Review ; review-article ; Stroke ; Therapeutic applications ; Transient receptor potential proteins ; Vaccine</subject><ispartof>Acta pharmacologica Sinica, 2018-05, Vol.39 (5), p.713-721</ispartof><rights>The Author(s) 2018</rights><rights>Copyright Nature Publishing Group May 2018</rights><rights>Copyright © 2018 The Author(s) 2018 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-3b54a13d36dbe097dd058e342c12071ac92438ea57491a548e9c162459495703</citedby><cites>FETCH-LOGICAL-c516t-3b54a13d36dbe097dd058e342c12071ac92438ea57491a548e9c162459495703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5943904/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5943904/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29542681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Turlova, Ekaterina</creatorcontrib><creatorcontrib>Feng, Zhong-ping</creatorcontrib><creatorcontrib>Sun, Hong-shuo</creatorcontrib><title>The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacol Sin</addtitle><description>Stroke is one of the major causes of mortality and morbidity worldwide, yet novel therapeutic treatments for this condition are lacking. This review focuses on the roles of the transient receptor potential melastatin 2 (TRPM2) ion channels in cellular damage following hypoxia-ischemia and their potential as a future therapeutic target for stroke. Here, we highlight the complex molecular signaling that takes place in neurons, glial cells and the blood-brain barrier following ischemic insult. We also describe the evidence of TRPM2 involvement in these processes, as shown from numerous
in vitro
and
in vivo
studies that utilize genetic and pharmacological approaches. This evidence implicates TRPM2 in a broad range of pathways that take place every stage of cerebral ischemic injury, thus making TRPM2 a promising target for drug development for stroke and other neurodegenerative conditions of the central nervous system.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Brain injury</subject><subject>Central nervous system</subject><subject>Drug development</subject><subject>Glial cells</subject><subject>Hypoxia</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Ion channels</subject><subject>Ischemia</subject><subject>Medical Microbiology</subject><subject>Molecular chains</subject><subject>Morbidity</subject><subject>Neuronal-glial interactions</subject><subject>Neurons</subject><subject>Pharmacology/Toxicology</subject><subject>Review</subject><subject>review-article</subject><subject>Stroke</subject><subject>Therapeutic applications</subject><subject>Transient receptor potential proteins</subject><subject>Vaccine</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1vEzEQxS0Eoh9w44wsceHQDf5cry9IqKKA1KoI5W55vZOsq40d7Cyi_z0TUkqLONny_OZ53jxCXnG24Ex27_y2LgTjZsGtekKOuVG6MUKrp3hvDW8U6-QROan1hjEpJLfPyZGwWom248ckL0egJU9A84ouv329EjSMPiWYKo2JJphLTvWMrqfoJxpgwnefBrrDtn7KeWj64hHsfSkRyr4nQAF8nGisYYRN9L8bxttt_hn9C_Js5acKL-_OU7K8-Lg8_9xcXn_6cv7hsgmat7tG9lp5LgfZDj0wa4aB6Q6kEoELZrgPVijZgddGWe616sAG3gqlrbLaMHlK3h9kt3O_gSFA2uFEblvixpdbl310jyspjm6dfzgUkJYpFHh7J1Dy9xnqzm3QDtr3CfJcHW5ccdyhbRF98w96k-eS0B1SUrXGdG2H1NmBCiXXWmB1Pwxnbh-kwyD3ssZhkIi_fmjgHv6THALNAahYSmsof3_9r-AvxRqnXw</recordid><startdate>20180501</startdate><enddate>20180501</enddate><creator>Turlova, Ekaterina</creator><creator>Feng, Zhong-ping</creator><creator>Sun, Hong-shuo</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180501</creationdate><title>The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia</title><author>Turlova, Ekaterina ; Feng, Zhong-ping ; Sun, Hong-shuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-3b54a13d36dbe097dd058e342c12071ac92438ea57491a548e9c162459495703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-brain barrier</topic><topic>Brain injury</topic><topic>Central nervous system</topic><topic>Drug development</topic><topic>Glial cells</topic><topic>Hypoxia</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Ion channels</topic><topic>Ischemia</topic><topic>Medical Microbiology</topic><topic>Molecular chains</topic><topic>Morbidity</topic><topic>Neuronal-glial interactions</topic><topic>Neurons</topic><topic>Pharmacology/Toxicology</topic><topic>Review</topic><topic>review-article</topic><topic>Stroke</topic><topic>Therapeutic applications</topic><topic>Transient receptor potential proteins</topic><topic>Vaccine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Turlova, Ekaterina</creatorcontrib><creatorcontrib>Feng, Zhong-ping</creatorcontrib><creatorcontrib>Sun, Hong-shuo</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Turlova, Ekaterina</au><au>Feng, Zhong-ping</au><au>Sun, Hong-shuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacol Sin</addtitle><date>2018-05-01</date><risdate>2018</risdate><volume>39</volume><issue>5</issue><spage>713</spage><epage>721</epage><pages>713-721</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Stroke is one of the major causes of mortality and morbidity worldwide, yet novel therapeutic treatments for this condition are lacking. This review focuses on the roles of the transient receptor potential melastatin 2 (TRPM2) ion channels in cellular damage following hypoxia-ischemia and their potential as a future therapeutic target for stroke. Here, we highlight the complex molecular signaling that takes place in neurons, glial cells and the blood-brain barrier following ischemic insult. We also describe the evidence of TRPM2 involvement in these processes, as shown from numerous
in vitro
and
in vivo
studies that utilize genetic and pharmacological approaches. This evidence implicates TRPM2 in a broad range of pathways that take place every stage of cerebral ischemic injury, thus making TRPM2 a promising target for drug development for stroke and other neurodegenerative conditions of the central nervous system.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29542681</pmid><doi>10.1038/aps.2017.194</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biomedical and Life Sciences Biomedicine Blood-brain barrier Brain injury Central nervous system Drug development Glial cells Hypoxia Immunology Internal Medicine Ion channels Ischemia Medical Microbiology Molecular chains Morbidity Neuronal-glial interactions Neurons Pharmacology/Toxicology Review review-article Stroke Therapeutic applications Transient receptor potential proteins Vaccine |
| title | The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia |
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