Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction
Sympathetic nervous system plays an important role in secondary injury of diseases. Accumulating evidence has observed association between ischemic stroke and renal dysfunction, but the mechanisms are incompletely clear. In this study, we investigated whether sympathetic hyperactivity can cause the...
Gespeichert in:
| Veröffentlicht in: | Translational stroke research 2022-08, Vol.13 (4), p.641-651 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 651 |
|---|---|
| container_issue | 4 |
| container_start_page | 641 |
| container_title | Translational stroke research |
| container_volume | 13 |
| creator | Cai, Yingyuan Lu, Xiaowei Cheng, Xi Lv, Qiushi Xu, Gelin Liu, Xinfeng |
| description | Sympathetic nervous system plays an important role in secondary injury of diseases. Accumulating evidence has observed association between ischemic stroke and renal dysfunction, but the mechanisms are incompletely clear. In this study, we investigated whether sympathetic hyperactivity can cause the development of renal dysfunction, apoptosis, and fibrogenesis after focal cerebral infarction. To determine the renal consequences of focal cerebral ischemia, we subjected a mice model of transient middle cerebral artery occlusion (tMCAO) and examined systolic blood pressure, heart rate, renal structure and function, serum catecholamine, and cortisol levels, and the expression of active caspase-3 bcl-2, bax, and phosphorylated p38 MAPK after 8 weeks. We also analyzed the relationship between insular cortex infarction and acute kidney injury (AKI) in 172 acute anterior circulation ischemic stroke (ACIS) patients. Transient right middle cerebral artery occlusion induced sympathetic hyperactivity, renal dysfunction, upregulation of apoptosis, and fibrogenesis in kidneys of mice. Metoprolol treatment relieves the development of renal injury. Study in stroke patients demonstrated that insular cortex infarction, especially the right insular cortex infarction, is an independent risk factor of AKI. Focal cerebral ischemia in mice leads to the development of renal injury driven by sympathetic hyperactivity. Right insular cortex infarction is an independent risk factor of AKI in older patients. Understanding the brain–kidney interaction after stroke would have clinical implications for the treatment and overall patient outcome. |
| doi_str_mv | 10.1007/s12975-021-00900-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2501266249</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2919439638</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-a0baa864713d05645018400a53e27db96ec4dd2d2f3fb165b86cf2a0bd86620d3</originalsourceid><addsrcrecordid>eNp9kU9rFDEYh4MottR-AQ8S8OKhY9_8mczMcdm6dqFQaCt4C5nknd0pu8mYzFjGT2_srgoezCUheX5PQn6EvGXwkQFUl4nxpioL4KwAaACKpxfklNWqLhSwry-PaylrcULOU3qEPASTSorX5ESIigngzSn5sfY2okno6B16s6NXc-omb8c--Au6GMIwhtSnC2q8o6u-jWGDHvMOfdjGMG229H7eD2bc4thbej0PGE0Of-_HmS66ESNdBZu1S4zYxrxY-87EZ_0b8qozu4Tnx_mMfFl9elheFze3n9fLxU1hRVWOhYHWmFrJ_GIHpZIlsFoCmFIgr1zbKLTSOe54J7qWqbKtle14TrlaKQ5OnJEPB-8Qw7cJ06j3fbK42xmPYUqaZyPPqGwy-v4f9DFMMX9LphrWSNEoUWeKHygbQ0oROz3Efm_irBnoX-XoQzk6l6Ofy9FPOfTuqJ7aPbo_kd9VZEAcgJSP_Abj37v_o_0JmmibYg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2919439638</pqid></control><display><type>article</type><title>Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction</title><source>ProQuest Central (Alumni Edition)</source><source>ProQuest Central UK/Ireland</source><source>SpringerLink Journals - AutoHoldings</source><source>ProQuest Central</source><creator>Cai, Yingyuan ; Lu, Xiaowei ; Cheng, Xi ; Lv, Qiushi ; Xu, Gelin ; Liu, Xinfeng</creator><creatorcontrib>Cai, Yingyuan ; Lu, Xiaowei ; Cheng, Xi ; Lv, Qiushi ; Xu, Gelin ; Liu, Xinfeng</creatorcontrib><description>Sympathetic nervous system plays an important role in secondary injury of diseases. Accumulating evidence has observed association between ischemic stroke and renal dysfunction, but the mechanisms are incompletely clear. In this study, we investigated whether sympathetic hyperactivity can cause the development of renal dysfunction, apoptosis, and fibrogenesis after focal cerebral infarction. To determine the renal consequences of focal cerebral ischemia, we subjected a mice model of transient middle cerebral artery occlusion (tMCAO) and examined systolic blood pressure, heart rate, renal structure and function, serum catecholamine, and cortisol levels, and the expression of active caspase-3 bcl-2, bax, and phosphorylated p38 MAPK after 8 weeks. We also analyzed the relationship between insular cortex infarction and acute kidney injury (AKI) in 172 acute anterior circulation ischemic stroke (ACIS) patients. Transient right middle cerebral artery occlusion induced sympathetic hyperactivity, renal dysfunction, upregulation of apoptosis, and fibrogenesis in kidneys of mice. Metoprolol treatment relieves the development of renal injury. Study in stroke patients demonstrated that insular cortex infarction, especially the right insular cortex infarction, is an independent risk factor of AKI. Focal cerebral ischemia in mice leads to the development of renal injury driven by sympathetic hyperactivity. Right insular cortex infarction is an independent risk factor of AKI in older patients. Understanding the brain–kidney interaction after stroke would have clinical implications for the treatment and overall patient outcome.</description><identifier>ISSN: 1868-4483</identifier><identifier>EISSN: 1868-601X</identifier><identifier>DOI: 10.1007/s12975-021-00900-w</identifier><identifier>PMID: 33713029</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adrenergic receptors ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cardiac arrhythmia ; Cardiology ; Carotid arteries ; Catecholamines ; Creatinine ; Drinking water ; Hormones ; Hospitals ; Hyperactivity ; Hyperglycemia ; Inflammation ; Ischemia ; Kidneys ; Laboratory animals ; Mortality ; Neurology ; Neurosciences ; Neurosurgery ; Original Article ; Proteins ; Stroke ; Surgery ; Traumatic brain injury ; Vascular Surgery ; Veins & arteries</subject><ispartof>Translational stroke research, 2022-08, Vol.13 (4), p.641-651</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-a0baa864713d05645018400a53e27db96ec4dd2d2f3fb165b86cf2a0bd86620d3</citedby><cites>FETCH-LOGICAL-c375t-a0baa864713d05645018400a53e27db96ec4dd2d2f3fb165b86cf2a0bd86620d3</cites><orcidid>0000-0002-8182-9632</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12975-021-00900-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2919439638?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,21388,21389,27924,27925,33530,33531,33744,33745,41488,42557,43659,43805,51319,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33713029$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cai, Yingyuan</creatorcontrib><creatorcontrib>Lu, Xiaowei</creatorcontrib><creatorcontrib>Cheng, Xi</creatorcontrib><creatorcontrib>Lv, Qiushi</creatorcontrib><creatorcontrib>Xu, Gelin</creatorcontrib><creatorcontrib>Liu, Xinfeng</creatorcontrib><title>Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction</title><title>Translational stroke research</title><addtitle>Transl. Stroke Res</addtitle><addtitle>Transl Stroke Res</addtitle><description>Sympathetic nervous system plays an important role in secondary injury of diseases. Accumulating evidence has observed association between ischemic stroke and renal dysfunction, but the mechanisms are incompletely clear. In this study, we investigated whether sympathetic hyperactivity can cause the development of renal dysfunction, apoptosis, and fibrogenesis after focal cerebral infarction. To determine the renal consequences of focal cerebral ischemia, we subjected a mice model of transient middle cerebral artery occlusion (tMCAO) and examined systolic blood pressure, heart rate, renal structure and function, serum catecholamine, and cortisol levels, and the expression of active caspase-3 bcl-2, bax, and phosphorylated p38 MAPK after 8 weeks. We also analyzed the relationship between insular cortex infarction and acute kidney injury (AKI) in 172 acute anterior circulation ischemic stroke (ACIS) patients. Transient right middle cerebral artery occlusion induced sympathetic hyperactivity, renal dysfunction, upregulation of apoptosis, and fibrogenesis in kidneys of mice. Metoprolol treatment relieves the development of renal injury. Study in stroke patients demonstrated that insular cortex infarction, especially the right insular cortex infarction, is an independent risk factor of AKI. Focal cerebral ischemia in mice leads to the development of renal injury driven by sympathetic hyperactivity. Right insular cortex infarction is an independent risk factor of AKI in older patients. Understanding the brain–kidney interaction after stroke would have clinical implications for the treatment and overall patient outcome.</description><subject>Adrenergic receptors</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiac arrhythmia</subject><subject>Cardiology</subject><subject>Carotid arteries</subject><subject>Catecholamines</subject><subject>Creatinine</subject><subject>Drinking water</subject><subject>Hormones</subject><subject>Hospitals</subject><subject>Hyperactivity</subject><subject>Hyperglycemia</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Kidneys</subject><subject>Laboratory animals</subject><subject>Mortality</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Original Article</subject><subject>Proteins</subject><subject>Stroke</subject><subject>Surgery</subject><subject>Traumatic brain injury</subject><subject>Vascular Surgery</subject><subject>Veins & arteries</subject><issn>1868-4483</issn><issn>1868-601X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kU9rFDEYh4MottR-AQ8S8OKhY9_8mczMcdm6dqFQaCt4C5nknd0pu8mYzFjGT2_srgoezCUheX5PQn6EvGXwkQFUl4nxpioL4KwAaACKpxfklNWqLhSwry-PaylrcULOU3qEPASTSorX5ESIigngzSn5sfY2okno6B16s6NXc-omb8c--Au6GMIwhtSnC2q8o6u-jWGDHvMOfdjGMG229H7eD2bc4thbej0PGE0Of-_HmS66ESNdBZu1S4zYxrxY-87EZ_0b8qozu4Tnx_mMfFl9elheFze3n9fLxU1hRVWOhYHWmFrJ_GIHpZIlsFoCmFIgr1zbKLTSOe54J7qWqbKtle14TrlaKQ5OnJEPB-8Qw7cJ06j3fbK42xmPYUqaZyPPqGwy-v4f9DFMMX9LphrWSNEoUWeKHygbQ0oROz3Efm_irBnoX-XoQzk6l6Ofy9FPOfTuqJ7aPbo_kd9VZEAcgJSP_Abj37v_o_0JmmibYg</recordid><startdate>20220801</startdate><enddate>20220801</enddate><creator>Cai, Yingyuan</creator><creator>Lu, Xiaowei</creator><creator>Cheng, Xi</creator><creator>Lv, Qiushi</creator><creator>Xu, Gelin</creator><creator>Liu, Xinfeng</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8182-9632</orcidid></search><sort><creationdate>20220801</creationdate><title>Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction</title><author>Cai, Yingyuan ; Lu, Xiaowei ; Cheng, Xi ; Lv, Qiushi ; Xu, Gelin ; Liu, Xinfeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-a0baa864713d05645018400a53e27db96ec4dd2d2f3fb165b86cf2a0bd86620d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adrenergic receptors</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardiac arrhythmia</topic><topic>Cardiology</topic><topic>Carotid arteries</topic><topic>Catecholamines</topic><topic>Creatinine</topic><topic>Drinking water</topic><topic>Hormones</topic><topic>Hospitals</topic><topic>Hyperactivity</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Kidneys</topic><topic>Laboratory animals</topic><topic>Mortality</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Original Article</topic><topic>Proteins</topic><topic>Stroke</topic><topic>Surgery</topic><topic>Traumatic brain injury</topic><topic>Vascular Surgery</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cai, Yingyuan</creatorcontrib><creatorcontrib>Lu, Xiaowei</creatorcontrib><creatorcontrib>Cheng, Xi</creatorcontrib><creatorcontrib>Lv, Qiushi</creatorcontrib><creatorcontrib>Xu, Gelin</creatorcontrib><creatorcontrib>Liu, Xinfeng</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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 One Psychology</collection><collection>MEDLINE - Academic</collection><jtitle>Translational stroke research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cai, Yingyuan</au><au>Lu, Xiaowei</au><au>Cheng, Xi</au><au>Lv, Qiushi</au><au>Xu, Gelin</au><au>Liu, Xinfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction</atitle><jtitle>Translational stroke research</jtitle><stitle>Transl. Stroke Res</stitle><addtitle>Transl Stroke Res</addtitle><date>2022-08-01</date><risdate>2022</risdate><volume>13</volume><issue>4</issue><spage>641</spage><epage>651</epage><pages>641-651</pages><issn>1868-4483</issn><eissn>1868-601X</eissn><abstract>Sympathetic nervous system plays an important role in secondary injury of diseases. Accumulating evidence has observed association between ischemic stroke and renal dysfunction, but the mechanisms are incompletely clear. In this study, we investigated whether sympathetic hyperactivity can cause the development of renal dysfunction, apoptosis, and fibrogenesis after focal cerebral infarction. To determine the renal consequences of focal cerebral ischemia, we subjected a mice model of transient middle cerebral artery occlusion (tMCAO) and examined systolic blood pressure, heart rate, renal structure and function, serum catecholamine, and cortisol levels, and the expression of active caspase-3 bcl-2, bax, and phosphorylated p38 MAPK after 8 weeks. We also analyzed the relationship between insular cortex infarction and acute kidney injury (AKI) in 172 acute anterior circulation ischemic stroke (ACIS) patients. Transient right middle cerebral artery occlusion induced sympathetic hyperactivity, renal dysfunction, upregulation of apoptosis, and fibrogenesis in kidneys of mice. Metoprolol treatment relieves the development of renal injury. Study in stroke patients demonstrated that insular cortex infarction, especially the right insular cortex infarction, is an independent risk factor of AKI. Focal cerebral ischemia in mice leads to the development of renal injury driven by sympathetic hyperactivity. Right insular cortex infarction is an independent risk factor of AKI in older patients. Understanding the brain–kidney interaction after stroke would have clinical implications for the treatment and overall patient outcome.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33713029</pmid><doi>10.1007/s12975-021-00900-w</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-8182-9632</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1868-4483 |
| ispartof | Translational stroke research, 2022-08, Vol.13 (4), p.641-651 |
| issn | 1868-4483 1868-601X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2501266249 |
| source | ProQuest Central (Alumni Edition); ProQuest Central UK/Ireland; SpringerLink Journals - AutoHoldings; ProQuest Central |
| subjects | Adrenergic receptors Apoptosis Biomedical and Life Sciences Biomedicine Cardiac arrhythmia Cardiology Carotid arteries Catecholamines Creatinine Drinking water Hormones Hospitals Hyperactivity Hyperglycemia Inflammation Ischemia Kidneys Laboratory animals Mortality Neurology Neurosciences Neurosurgery Original Article Proteins Stroke Surgery Traumatic brain injury Vascular Surgery Veins & arteries |
| title | Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T19%3A41%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Increased%20Renal%20Dysfunction,%20Apoptosis,%20and%20Fibrogenesis%20Through%20Sympathetic%20Hyperactivity%20After%20Focal%20Cerebral%20Infarction&rft.jtitle=Translational%20stroke%20research&rft.au=Cai,%20Yingyuan&rft.date=2022-08-01&rft.volume=13&rft.issue=4&rft.spage=641&rft.epage=651&rft.pages=641-651&rft.issn=1868-4483&rft.eissn=1868-601X&rft_id=info:doi/10.1007/s12975-021-00900-w&rft_dat=%3Cproquest_cross%3E2919439638%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2919439638&rft_id=info:pmid/33713029&rfr_iscdi=true |