Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential
Background Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear. Objective To summarize the cur...
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| Veröffentlicht in: | Cardiovascular drugs and therapy 2024-10, Vol.38 (5), p.999-1015 |
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| creator | Liu, Leiling Hu, Jiahui Lei, Hao Qin, Huali Wang, Chunfang Gui, Yajun Xu, Danyan |
| description | Background
Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear.
Objective
To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach.
Results
Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability.
Conclusion
Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy. |
| doi_str_mv | 10.1007/s10557-023-07463-y |
| format | Article |
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Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear.
Objective
To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach.
Results
Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability.
Conclusion
Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy.</description><identifier>ISSN: 0920-3206</identifier><identifier>ISSN: 1573-7241</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1007/s10557-023-07463-y</identifier><identifier>PMID: 37184744</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Aorta ; Aortic stenosis ; Cardiology ; Cardiomegaly - immunology ; Cardiomegaly - pathology ; Cardiomegaly - physiopathology ; Cardiomegaly - therapy ; Cardiomyopathy ; Chronic obstructive pulmonary disease ; Clinical trials ; Coronary artery disease ; Diabetes mellitus ; Heart diseases ; Humans ; Hypertension ; Hypertrophy ; Immunoregulation ; Immunosuppressive agents ; Inflammation ; Inflammatory response ; Lung diseases ; Lymphocytes ; Lymphocytes T ; Medicine ; Medicine & Public Health ; Metabolic disorders ; Myocardial infarction ; Myocarditis ; Review Article ; Storage diseases ; T-Lymphocytes, Regulatory - immunology</subject><ispartof>Cardiovascular drugs and therapy, 2024-10, Vol.38 (5), p.999-1015</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-5ebee2dea44bb8a7304f377cc598789a1b4c080219828f2edfbd88c59f086a083</citedby><cites>FETCH-LOGICAL-c375t-5ebee2dea44bb8a7304f377cc598789a1b4c080219828f2edfbd88c59f086a083</cites><orcidid>0000-0003-2113-0800</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/s10557-023-07463-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10557-023-07463-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37184744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Leiling</creatorcontrib><creatorcontrib>Hu, Jiahui</creatorcontrib><creatorcontrib>Lei, Hao</creatorcontrib><creatorcontrib>Qin, Huali</creatorcontrib><creatorcontrib>Wang, Chunfang</creatorcontrib><creatorcontrib>Gui, Yajun</creatorcontrib><creatorcontrib>Xu, Danyan</creatorcontrib><title>Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential</title><title>Cardiovascular drugs and therapy</title><addtitle>Cardiovasc Drugs Ther</addtitle><addtitle>Cardiovasc Drugs Ther</addtitle><description>Background
Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear.
Objective
To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach.
Results
Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability.
Conclusion
Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy.</description><subject>Animals</subject><subject>Aorta</subject><subject>Aortic stenosis</subject><subject>Cardiology</subject><subject>Cardiomegaly - immunology</subject><subject>Cardiomegaly - pathology</subject><subject>Cardiomegaly - physiopathology</subject><subject>Cardiomegaly - therapy</subject><subject>Cardiomyopathy</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Clinical trials</subject><subject>Coronary artery disease</subject><subject>Diabetes mellitus</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Immunoregulation</subject><subject>Immunosuppressive agents</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Lung diseases</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic disorders</subject><subject>Myocardial infarction</subject><subject>Myocarditis</subject><subject>Review Article</subject><subject>Storage diseases</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><issn>0920-3206</issn><issn>1573-7241</issn><issn>1573-7241</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD1v2zAQhokgRewk_QMdAgJZuig9fsiksgVGWgdIUaNwtgIERZ1sBbKokNKgf1-2dhMgQycO97zv8R5CPjG4YQDqS2SQ5yoDLjJQciGy6YTMWa5Eprhkp2QOBYdMcFjMyHmMz5BCRaHPyEwopqWSck5-_cTt2NrBh4lu6BLbNtKmo2s77Hzrt42zLV3aUDXW0dXUYxiC73fTLf2Obme7Ju4jtV1FNzsMtsdxaBxd-wG7obHtJflQ2zbix-N7QZ6-3m-Wq-zxx7eH5d1j5oTKhyzHEpFXaKUsS22VAFkLpZzLC610YVkpHWjgrNBc1xyruqy0TtMa9MKCFhfk86G3D_5lxDiYfRNdusV26MdouGZCa1kwldDrd-izH0OXfmcEY6AZWyiRKH6gXPAxBqxNH5q9DZNhYP64Nwf3Jrk3f92bKYWujtVjucfqNfJPdgLEAYhp1G0xvO3-T-1vuQ6Pvg</recordid><startdate>20241001</startdate><enddate>20241001</enddate><creator>Liu, Leiling</creator><creator>Hu, Jiahui</creator><creator>Lei, Hao</creator><creator>Qin, Huali</creator><creator>Wang, Chunfang</creator><creator>Gui, Yajun</creator><creator>Xu, Danyan</creator><general>Springer US</general><general>Springer Nature B.V</general><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>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2113-0800</orcidid></search><sort><creationdate>20241001</creationdate><title>Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential</title><author>Liu, Leiling ; Hu, Jiahui ; Lei, Hao ; Qin, Huali ; Wang, Chunfang ; Gui, Yajun ; Xu, Danyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-5ebee2dea44bb8a7304f377cc598789a1b4c080219828f2edfbd88c59f086a083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Aorta</topic><topic>Aortic stenosis</topic><topic>Cardiology</topic><topic>Cardiomegaly - immunology</topic><topic>Cardiomegaly - pathology</topic><topic>Cardiomegaly - physiopathology</topic><topic>Cardiomegaly - therapy</topic><topic>Cardiomyopathy</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Clinical trials</topic><topic>Coronary artery disease</topic><topic>Diabetes mellitus</topic><topic>Heart diseases</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertrophy</topic><topic>Immunoregulation</topic><topic>Immunosuppressive agents</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Lung diseases</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic disorders</topic><topic>Myocardial infarction</topic><topic>Myocarditis</topic><topic>Review Article</topic><topic>Storage diseases</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Leiling</creatorcontrib><creatorcontrib>Hu, Jiahui</creatorcontrib><creatorcontrib>Lei, Hao</creatorcontrib><creatorcontrib>Qin, Huali</creatorcontrib><creatorcontrib>Wang, Chunfang</creatorcontrib><creatorcontrib>Gui, Yajun</creatorcontrib><creatorcontrib>Xu, Danyan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Leiling</au><au>Hu, Jiahui</au><au>Lei, Hao</au><au>Qin, Huali</au><au>Wang, Chunfang</au><au>Gui, Yajun</au><au>Xu, Danyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><stitle>Cardiovasc Drugs Ther</stitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>2024-10-01</date><risdate>2024</risdate><volume>38</volume><issue>5</issue><spage>999</spage><epage>1015</epage><pages>999-1015</pages><issn>0920-3206</issn><issn>1573-7241</issn><eissn>1573-7241</eissn><abstract>Background
Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear.
Objective
To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach.
Results
Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability.
Conclusion
Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37184744</pmid><doi>10.1007/s10557-023-07463-y</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0003-2113-0800</orcidid></addata></record> |
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| subjects | Animals Aorta Aortic stenosis Cardiology Cardiomegaly - immunology Cardiomegaly - pathology Cardiomegaly - physiopathology Cardiomegaly - therapy Cardiomyopathy Chronic obstructive pulmonary disease Clinical trials Coronary artery disease Diabetes mellitus Heart diseases Humans Hypertension Hypertrophy Immunoregulation Immunosuppressive agents Inflammation Inflammatory response Lung diseases Lymphocytes Lymphocytes T Medicine Medicine & Public Health Metabolic disorders Myocardial infarction Myocarditis Review Article Storage diseases T-Lymphocytes, Regulatory - immunology |
| title | Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential |
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