Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats
It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel th...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular and molecular medicine 2021-09, Vol.25 (18), p.8997-9010 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 9010 |
|---|---|
| container_issue | 18 |
| container_start_page | 8997 |
| container_title | Journal of cellular and molecular medicine |
| container_volume | 25 |
| creator | Nie, Chaoqun Zou, Rentong Pan, Shuang A, Rong Gao, Yunan Yang, Hongxiao Bai, Juncai Xi, Shuiqing Wang, Xue Hong, Xiaojian Yang, Wei |
| description | It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis. |
| doi_str_mv | 10.1111/jcmm.16863 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_webof</sourceid><recordid>TN_cdi_proquest_miscellaneous_2562234563</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2571752543</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4483-7e5a6bad4ec6bef78585d2bf18b03258b281bb27f136864e6963090964fbffe43</originalsourceid><addsrcrecordid>eNqNkU2LFDEQhhtR3HX14g-QBi-izJrvTl8EGdRVZlVEzyFJV2azdJI16Vbm7B838-GgHsRcUqGeeqtSb9M8xOgc1_P82oZwjoUU9FZzirkkC9ZTdvsQY0nlSXOvlGuEqMC0v9ucUMYQwYKdNj8uNkNOa4jtWpfWxys96smn2OoAo09ZT1Baq_PgtW0zhDTAOPq4bnUcWudNTsWX1mxqbj1vS2vq_erTR1q13KhD0CUFqI82bNJeZ9ymdLa7NrVBud_ccXos8OBwnzVfXr_6vLxYrD68ebt8uVpYxiRddMC1MHpgYIUB10ku-UCMw9IgSrg0RGJjSOcwrbtgIHpBUY96wZxxDhg9a17sdW9mE2CwEKesR3WTfdB5o5L26s9M9Fdqnb4pyShnmFSBJweBnL7OUCYVfLF1ITpCmosiXBBCGRe0oo__Qq_TnGP9XqU63HHC2ZZ6uqds3WPJ4I7DYKS23qqtt2rnbYUf_T7-Ef1lZgXkHvgOJrliPUQLRwwhJCTvCe5qhPDSTzujl2mOUy199v-llcYH2o-w-cfM6t3y8nI__U8l39Kz</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2571752543</pqid></control><display><type>article</type><title>Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Access via Wiley Online Library</source><source>Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /></source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Nie, Chaoqun ; Zou, Rentong ; Pan, Shuang ; A, Rong ; Gao, Yunan ; Yang, Hongxiao ; Bai, Juncai ; Xi, Shuiqing ; Wang, Xue ; Hong, Xiaojian ; Yang, Wei</creator><creatorcontrib>Nie, Chaoqun ; Zou, Rentong ; Pan, Shuang ; A, Rong ; Gao, Yunan ; Yang, Hongxiao ; Bai, Juncai ; Xi, Shuiqing ; Wang, Xue ; Hong, Xiaojian ; Yang, Wei</creatorcontrib><description>It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.16863</identifier><identifier>PMID: 34402164</identifier><language>eng</language><publisher>HOBOKEN: Wiley</publisher><subject>Angiotensin ; Angiotensin II ; Animals ; Bioengineering ; Cardiac function ; cardiac remodelling ; Cardiomyocytes ; Cell Biology ; Congestive heart failure ; Fibroblasts ; Fibrosis ; Fibrosis - drug therapy ; Heart attacks ; Heart failure ; Heart Failure - drug therapy ; Hydrogen ; Hydrogen - pharmacology ; Hydrogen - therapeutic use ; Hypoxia ; Inflammasomes ; Inflammation ; Inhalation ; Ischemia ; Life Sciences & Biomedicine ; Male ; Medicine, Research & Experimental ; Myocardial infarction ; Myocytes, Cardiac ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Original ; Ostomy ; Oxidative stress ; Primary Cell Culture ; Pyroptosis ; Quality of life ; Rats ; Rats, Sprague-Dawley ; Research & Experimental Medicine ; Science & Technology ; Ultrasonic imaging ; Ventricular Remodeling - drug effects</subject><ispartof>Journal of cellular and molecular medicine, 2021-09, Vol.25 (18), p.8997-9010</ispartof><rights>2021 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>16</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000685921700001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c4483-7e5a6bad4ec6bef78585d2bf18b03258b281bb27f136864e6963090964fbffe43</citedby><cites>FETCH-LOGICAL-c4483-7e5a6bad4ec6bef78585d2bf18b03258b281bb27f136864e6963090964fbffe43</cites><orcidid>0000-0001-7245-4579 ; 0000-0003-2405-1913 ; 0000-0002-2992-3074</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435412/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435412/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,2115,11567,27929,27930,39263,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34402164$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nie, Chaoqun</creatorcontrib><creatorcontrib>Zou, Rentong</creatorcontrib><creatorcontrib>Pan, Shuang</creatorcontrib><creatorcontrib>A, Rong</creatorcontrib><creatorcontrib>Gao, Yunan</creatorcontrib><creatorcontrib>Yang, Hongxiao</creatorcontrib><creatorcontrib>Bai, Juncai</creatorcontrib><creatorcontrib>Xi, Shuiqing</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Hong, Xiaojian</creatorcontrib><creatorcontrib>Yang, Wei</creatorcontrib><title>Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats</title><title>Journal of cellular and molecular medicine</title><addtitle>J CELL MOL MED</addtitle><addtitle>J Cell Mol Med</addtitle><description>It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Animals</subject><subject>Bioengineering</subject><subject>Cardiac function</subject><subject>cardiac remodelling</subject><subject>Cardiomyocytes</subject><subject>Cell Biology</subject><subject>Congestive heart failure</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Fibrosis - drug therapy</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Heart Failure - drug therapy</subject><subject>Hydrogen</subject><subject>Hydrogen - pharmacology</subject><subject>Hydrogen - therapeutic use</subject><subject>Hypoxia</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Inhalation</subject><subject>Ischemia</subject><subject>Life Sciences & Biomedicine</subject><subject>Male</subject><subject>Medicine, Research & Experimental</subject><subject>Myocardial infarction</subject><subject>Myocytes, Cardiac</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Original</subject><subject>Ostomy</subject><subject>Oxidative stress</subject><subject>Primary Cell Culture</subject><subject>Pyroptosis</subject><subject>Quality of life</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Research & Experimental Medicine</subject><subject>Science & Technology</subject><subject>Ultrasonic imaging</subject><subject>Ventricular Remodeling - drug effects</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU2LFDEQhhtR3HX14g-QBi-izJrvTl8EGdRVZlVEzyFJV2azdJI16Vbm7B838-GgHsRcUqGeeqtSb9M8xOgc1_P82oZwjoUU9FZzirkkC9ZTdvsQY0nlSXOvlGuEqMC0v9ucUMYQwYKdNj8uNkNOa4jtWpfWxys96smn2OoAo09ZT1Baq_PgtW0zhDTAOPq4bnUcWudNTsWX1mxqbj1vS2vq_erTR1q13KhD0CUFqI82bNJeZ9ymdLa7NrVBud_ccXos8OBwnzVfXr_6vLxYrD68ebt8uVpYxiRddMC1MHpgYIUB10ku-UCMw9IgSrg0RGJjSOcwrbtgIHpBUY96wZxxDhg9a17sdW9mE2CwEKesR3WTfdB5o5L26s9M9Fdqnb4pyShnmFSBJweBnL7OUCYVfLF1ITpCmosiXBBCGRe0oo__Qq_TnGP9XqU63HHC2ZZ6uqds3WPJ4I7DYKS23qqtt2rnbYUf_T7-Ef1lZgXkHvgOJrliPUQLRwwhJCTvCe5qhPDSTzujl2mOUy199v-llcYH2o-w-cfM6t3y8nI__U8l39Kz</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Nie, Chaoqun</creator><creator>Zou, Rentong</creator><creator>Pan, Shuang</creator><creator>A, Rong</creator><creator>Gao, Yunan</creator><creator>Yang, Hongxiao</creator><creator>Bai, Juncai</creator><creator>Xi, Shuiqing</creator><creator>Wang, Xue</creator><creator>Hong, Xiaojian</creator><creator>Yang, Wei</creator><general>Wiley</general><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7245-4579</orcidid><orcidid>https://orcid.org/0000-0003-2405-1913</orcidid><orcidid>https://orcid.org/0000-0002-2992-3074</orcidid></search><sort><creationdate>202109</creationdate><title>Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats</title><author>Nie, Chaoqun ; Zou, Rentong ; Pan, Shuang ; A, Rong ; Gao, Yunan ; Yang, Hongxiao ; Bai, Juncai ; Xi, Shuiqing ; Wang, Xue ; Hong, Xiaojian ; Yang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-7e5a6bad4ec6bef78585d2bf18b03258b281bb27f136864e6963090964fbffe43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Animals</topic><topic>Bioengineering</topic><topic>Cardiac function</topic><topic>cardiac remodelling</topic><topic>Cardiomyocytes</topic><topic>Cell Biology</topic><topic>Congestive heart failure</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Fibrosis - drug therapy</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>Heart Failure - drug therapy</topic><topic>Hydrogen</topic><topic>Hydrogen - pharmacology</topic><topic>Hydrogen - therapeutic use</topic><topic>Hypoxia</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Inhalation</topic><topic>Ischemia</topic><topic>Life Sciences & Biomedicine</topic><topic>Male</topic><topic>Medicine, Research & Experimental</topic><topic>Myocardial infarction</topic><topic>Myocytes, Cardiac</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Original</topic><topic>Ostomy</topic><topic>Oxidative stress</topic><topic>Primary Cell Culture</topic><topic>Pyroptosis</topic><topic>Quality of life</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Research & Experimental Medicine</topic><topic>Science & Technology</topic><topic>Ultrasonic imaging</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nie, Chaoqun</creatorcontrib><creatorcontrib>Zou, Rentong</creatorcontrib><creatorcontrib>Pan, Shuang</creatorcontrib><creatorcontrib>A, Rong</creatorcontrib><creatorcontrib>Gao, Yunan</creatorcontrib><creatorcontrib>Yang, Hongxiao</creatorcontrib><creatorcontrib>Bai, Juncai</creatorcontrib><creatorcontrib>Xi, Shuiqing</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Hong, Xiaojian</creatorcontrib><creatorcontrib>Yang, Wei</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 (ProQuest)</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>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>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nie, Chaoqun</au><au>Zou, Rentong</au><au>Pan, Shuang</au><au>A, Rong</au><au>Gao, Yunan</au><au>Yang, Hongxiao</au><au>Bai, Juncai</au><au>Xi, Shuiqing</au><au>Wang, Xue</au><au>Hong, Xiaojian</au><au>Yang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><stitle>J CELL MOL MED</stitle><addtitle>J Cell Mol Med</addtitle><date>2021-09</date><risdate>2021</risdate><volume>25</volume><issue>18</issue><spage>8997</spage><epage>9010</epage><pages>8997-9010</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis.</abstract><cop>HOBOKEN</cop><pub>Wiley</pub><pmid>34402164</pmid><doi>10.1111/jcmm.16863</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7245-4579</orcidid><orcidid>https://orcid.org/0000-0003-2405-1913</orcidid><orcidid>https://orcid.org/0000-0002-2992-3074</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1582-1838 |
| ispartof | Journal of cellular and molecular medicine, 2021-09, Vol.25 (18), p.8997-9010 |
| issn | 1582-1838 1582-4934 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2562234563 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Angiotensin Angiotensin II Animals Bioengineering Cardiac function cardiac remodelling Cardiomyocytes Cell Biology Congestive heart failure Fibroblasts Fibrosis Fibrosis - drug therapy Heart attacks Heart failure Heart Failure - drug therapy Hydrogen Hydrogen - pharmacology Hydrogen - therapeutic use Hypoxia Inflammasomes Inflammation Inhalation Ischemia Life Sciences & Biomedicine Male Medicine, Research & Experimental Myocardial infarction Myocytes, Cardiac NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Original Ostomy Oxidative stress Primary Cell Culture Pyroptosis Quality of life Rats Rats, Sprague-Dawley Research & Experimental Medicine Science & Technology Ultrasonic imaging Ventricular Remodeling - drug effects |
| title | Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-12T12%3A39%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_webof&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hydrogen%20gas%20inhalation%20ameliorates%20cardiac%20remodelling%20and%20fibrosis%20by%20regulating%20NLRP3%20inflammasome%20in%20myocardial%20infarction%20rats&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Nie,%20Chaoqun&rft.date=2021-09&rft.volume=25&rft.issue=18&rft.spage=8997&rft.epage=9010&rft.pages=8997-9010&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.16863&rft_dat=%3Cproquest_webof%3E2571752543%3C/proquest_webof%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2571752543&rft_id=info:pmid/34402164&rfr_iscdi=true |