Targeting Immune Senescence in Atherosclerosis
Atherosclerosis is one of the main underlying causes of cardiovascular diseases (CVD). It is associated with chronic inflammation and intimal thickening as well as the involvement of multiple cell types including immune cells. The engagement of innate or adaptive immune response has either athero-pr...
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| Veröffentlicht in: | International journal of molecular sciences 2022-11, Vol.23 (21), p.13059 |
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| description | Atherosclerosis is one of the main underlying causes of cardiovascular diseases (CVD). It is associated with chronic inflammation and intimal thickening as well as the involvement of multiple cell types including immune cells. The engagement of innate or adaptive immune response has either athero-protective or atherogenic properties in exacerbating or alleviating atherosclerosis. In atherosclerosis, the mechanism of action of immune cells, particularly monocytes, macrophages, dendritic cells, and B- and T-lymphocytes have been discussed. Immuno-senescence is associated with aging, viral infections, genetic predispositions, and hyperlipidemia, which contribute to atherosclerosis. Immune senescent cells secrete SASP that delays or accelerates atherosclerosis plaque growth and associated pathologies such as aneurysms and coronary artery disease. Senescent cells undergo cell cycle arrest, morphological changes, and phenotypic changes in terms of their abundances and secretome profile including cytokines, chemokines, matrix metalloproteases (MMPs) and Toll-like receptors (TLRs) expressions. The senescence markers are used in therapeutics and currently, senolytics represent one of the emerging treatments where specific targets and clearance of senescent cells are being considered as therapy targets for the prevention or treatment of atherosclerosis. |
| doi_str_mv | 10.3390/ijms232113059 |
| format | Article |
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It is associated with chronic inflammation and intimal thickening as well as the involvement of multiple cell types including immune cells. The engagement of innate or adaptive immune response has either athero-protective or atherogenic properties in exacerbating or alleviating atherosclerosis. In atherosclerosis, the mechanism of action of immune cells, particularly monocytes, macrophages, dendritic cells, and B- and T-lymphocytes have been discussed. Immuno-senescence is associated with aging, viral infections, genetic predispositions, and hyperlipidemia, which contribute to atherosclerosis. Immune senescent cells secrete SASP that delays or accelerates atherosclerosis plaque growth and associated pathologies such as aneurysms and coronary artery disease. Senescent cells undergo cell cycle arrest, morphological changes, and phenotypic changes in terms of their abundances and secretome profile including cytokines, chemokines, matrix metalloproteases (MMPs) and Toll-like receptors (TLRs) expressions. The senescence markers are used in therapeutics and currently, senolytics represent one of the emerging treatments where specific targets and clearance of senescent cells are being considered as therapy targets for the prevention or treatment of atherosclerosis.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms232113059</identifier><identifier>PMID: 36361845</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Adaptive immunity ; Aging ; Angina pectoris ; Antibodies ; Antigens ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Blood vessels ; Cardiovascular disease ; Cardiovascular diseases ; Cell cycle ; Chemokines ; Collagen ; Coronary artery disease ; Coronary vessels ; Cytokines ; Cytotoxicity ; Dendritic cells ; Extracellular matrix ; Heart attacks ; Heart diseases ; Hyperlipidemia ; Immune clearance ; Immune system ; Inflammation ; Lipids ; Lymphocytes ; Lymphocytes T ; Macrophages ; Monocytes ; Review ; Secretome ; Senescence ; Smooth muscle ; Thickening ; Toll-like receptors</subject><ispartof>International journal of molecular sciences, 2022-11, Vol.23 (21), p.13059</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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It is associated with chronic inflammation and intimal thickening as well as the involvement of multiple cell types including immune cells. The engagement of innate or adaptive immune response has either athero-protective or atherogenic properties in exacerbating or alleviating atherosclerosis. In atherosclerosis, the mechanism of action of immune cells, particularly monocytes, macrophages, dendritic cells, and B- and T-lymphocytes have been discussed. Immuno-senescence is associated with aging, viral infections, genetic predispositions, and hyperlipidemia, which contribute to atherosclerosis. Immune senescent cells secrete SASP that delays or accelerates atherosclerosis plaque growth and associated pathologies such as aneurysms and coronary artery disease. Senescent cells undergo cell cycle arrest, morphological changes, and phenotypic changes in terms of their abundances and secretome profile including cytokines, chemokines, matrix metalloproteases (MMPs) and Toll-like receptors (TLRs) expressions. The senescence markers are used in therapeutics and currently, senolytics represent one of the emerging treatments where specific targets and clearance of senescent cells are being considered as therapy targets for the prevention or treatment of atherosclerosis.</description><subject>Adaptive immunity</subject><subject>Aging</subject><subject>Angina pectoris</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Blood vessels</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cell cycle</subject><subject>Chemokines</subject><subject>Collagen</subject><subject>Coronary artery disease</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Dendritic cells</subject><subject>Extracellular matrix</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Hyperlipidemia</subject><subject>Immune clearance</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Lipids</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Monocytes</subject><subject>Review</subject><subject>Secretome</subject><subject>Senescence</subject><subject>Smooth muscle</subject><subject>Thickening</subject><subject>Toll-like receptors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkU1LAzEQhoMotlaP3gtevGzNdzYXoRQ_CgUP1nNId2fblN1sTXYF_70pLWKdw8zAPLzMO4PQLcETxjR-cNsmUkYJYVjoMzQknNIMY6nO__QDdBXjFuMECn2JBkwySXIuhmiytGENnfPr8bxpeg_jd_AQC_AFjJ0fT7sNhDYW9T67eI0uKltHuDnWEfp4flrOXrPF28t8Nl1kBdO0y0hZCbqSlAPjFRYEWKmLQmlMVIVVCqkl13me8xXlTChQ1GoB2IqyYqKo2Ag9HnR3_aqBMq3TBVubXXCNDd-mtc6cTrzbmHX7ZbQUOSM6CdwfBUL72UPsTOOSq7q2Hto-GqqYyKVQiR6hu3_otu2DT_b2FJfJEZGJyg5UkQ4RA1S_yxBs9p8wJ59gPygoeVo</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Vellasamy, Danusha Michelle</creator><creator>Lee, Sin-Jye</creator><creator>Goh, Khang Wen</creator><creator>Goh, Bey-Hing</creator><creator>Tang, Yin-Quan</creator><creator>Ming, Long Chiau</creator><creator>Yap, Wei Hsum</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8116-6018</orcidid><orcidid>https://orcid.org/0000-0003-1006-3649</orcidid><orcidid>https://orcid.org/0000-0002-6971-1383</orcidid><orcidid>https://orcid.org/0000-0001-7327-2830</orcidid><orcidid>https://orcid.org/0000-0001-6686-7019</orcidid></search><sort><creationdate>20221101</creationdate><title>Targeting Immune Senescence in Atherosclerosis</title><author>Vellasamy, Danusha Michelle ; 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Senescent cells undergo cell cycle arrest, morphological changes, and phenotypic changes in terms of their abundances and secretome profile including cytokines, chemokines, matrix metalloproteases (MMPs) and Toll-like receptors (TLRs) expressions. The senescence markers are used in therapeutics and currently, senolytics represent one of the emerging treatments where specific targets and clearance of senescent cells are being considered as therapy targets for the prevention or treatment of atherosclerosis.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>36361845</pmid><doi>10.3390/ijms232113059</doi><orcidid>https://orcid.org/0000-0001-8116-6018</orcidid><orcidid>https://orcid.org/0000-0003-1006-3649</orcidid><orcidid>https://orcid.org/0000-0002-6971-1383</orcidid><orcidid>https://orcid.org/0000-0001-7327-2830</orcidid><orcidid>https://orcid.org/0000-0001-6686-7019</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptive immunity Aging Angina pectoris Antibodies Antigens Apoptosis Arteriosclerosis Atherosclerosis Blood vessels Cardiovascular disease Cardiovascular diseases Cell cycle Chemokines Collagen Coronary artery disease Coronary vessels Cytokines Cytotoxicity Dendritic cells Extracellular matrix Heart attacks Heart diseases Hyperlipidemia Immune clearance Immune system Inflammation Lipids Lymphocytes Lymphocytes T Macrophages Monocytes Review Secretome Senescence Smooth muscle Thickening Toll-like receptors |
| title | Targeting Immune Senescence in Atherosclerosis |
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