Advances in the study of S100A9 in cardiovascular diseases
Cardiovascular disease (CVD) is a group of diseases that primarily affect the heart or blood vessels, with high disability and mortality rates, posing a serious threat to human health. The causative factors, pathogenesis, and characteristics of common CVD differ, but they all involve common patholog...
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description | Cardiovascular disease (CVD) is a group of diseases that primarily affect the heart or blood vessels, with high disability and mortality rates, posing a serious threat to human health. The causative factors, pathogenesis, and characteristics of common CVD differ, but they all involve common pathological processes such as inflammation, oxidative stress, and fibrosis. S100A9 belongs to the S100 family of calcium‐binding proteins, which are mainly secreted by myeloid cells and bind to the Toll‐like receptor 4 and receptor for advanced glycation end products and is involved in regulating pathological processes such as inflammatory response, fibrosis, vascular calcification, and endothelial barrier function in CVD. The latest research has found that S100A9 is a key biomarker for diagnosing and predicting various CVD. Therefore, this article reviews the latest research progress on the diagnostic and predictive, and therapeutic value of S100A9 in inflammatory‐related CVD such as atherosclerosis, myocardial infarction, and arterial aneurysm and summarizes its molecular mechanisms in the progression of CVD, aiming to explore new predictive methods and to identify potential intervention targets for CVD in clinical practice.
S100A9 is released by immune and tissue cells in response to stressors such as damage, inflammation, and oxidative stress. This leads to the amplification of inflammation, anti‐inflammatory effects, induction of endothelial dysfunction, promotion of vascular microcalcification, as well as stimulation of cell proliferation, autophagy, apoptosis, and death. S100A9 can serve as a biomarker for diagnosis, prediction, and evaluation of cardiovascular diseases, and it is also considered a potential therapeutic target. |
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S100A9 is released by immune and tissue cells in response to stressors such as damage, inflammation, and oxidative stress. This leads to the amplification of inflammation, anti‐inflammatory effects, induction of endothelial dysfunction, promotion of vascular microcalcification, as well as stimulation of cell proliferation, autophagy, apoptosis, and death. S100A9 can serve as a biomarker for diagnosis, prediction, and evaluation of cardiovascular diseases, and it is also considered a potential therapeutic target.</description><identifier>ISSN: 0960-7722</identifier><identifier>ISSN: 1365-2184</identifier><identifier>EISSN: 1365-2184</identifier><identifier>DOI: 10.1111/cpr.13636</identifier><identifier>PMID: 38504474</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Advanced glycosylation end products ; Aneurysms ; Animals ; Arteriosclerosis ; Atherosclerosis ; Biomarkers ; Biomarkers - metabolism ; Blood vessels ; Calcification ; Calcification (ectopic) ; Calgranulin B - metabolism ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular disease ; Cardiovascular diseases ; Cardiovascular Diseases - metabolism ; Chemokines ; Cytokines ; Dendritic cells ; Fibroblasts ; Fibrosis ; Heart attacks ; Heart diseases ; Humans ; Inflammation ; Inflammation - metabolism ; Inflammatory response ; Leukocytes ; Molecular modelling ; Myeloid cells ; Myocardial infarction ; Myocarditis ; Neutrophils ; Oxidative Stress ; Pathogenesis ; Physiology ; Preeclampsia ; Proteins ; Pulmonary hypertension ; Review ; TLR4 protein ; Toll-like receptors</subject><ispartof>Cell proliferation, 2024-08, Vol.57 (8), p.e13636-n/a</ispartof><rights>2024 The Authors. published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.</rights><rights>2024 The Authors. Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.</rights><rights>2024. 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>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4046-d10713916a6e75641cbfd725b321dd11bab748d66e1d5ad50e6bec6c8f822d953</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/PMC11294427/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294427/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46031,46455,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38504474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Fengling</creatorcontrib><creatorcontrib>He, Ziyu</creatorcontrib><creatorcontrib>Wang, Chengming</creatorcontrib><creatorcontrib>Si, Jiajia</creatorcontrib><creatorcontrib>Chen, Zhu</creatorcontrib><creatorcontrib>Guo, Yuan</creatorcontrib><title>Advances in the study of S100A9 in cardiovascular diseases</title><title>Cell proliferation</title><addtitle>Cell Prolif</addtitle><description>Cardiovascular disease (CVD) is a group of diseases that primarily affect the heart or blood vessels, with high disability and mortality rates, posing a serious threat to human health. The causative factors, pathogenesis, and characteristics of common CVD differ, but they all involve common pathological processes such as inflammation, oxidative stress, and fibrosis. S100A9 belongs to the S100 family of calcium‐binding proteins, which are mainly secreted by myeloid cells and bind to the Toll‐like receptor 4 and receptor for advanced glycation end products and is involved in regulating pathological processes such as inflammatory response, fibrosis, vascular calcification, and endothelial barrier function in CVD. The latest research has found that S100A9 is a key biomarker for diagnosing and predicting various CVD. Therefore, this article reviews the latest research progress on the diagnostic and predictive, and therapeutic value of S100A9 in inflammatory‐related CVD such as atherosclerosis, myocardial infarction, and arterial aneurysm and summarizes its molecular mechanisms in the progression of CVD, aiming to explore new predictive methods and to identify potential intervention targets for CVD in clinical practice.
S100A9 is released by immune and tissue cells in response to stressors such as damage, inflammation, and oxidative stress. This leads to the amplification of inflammation, anti‐inflammatory effects, induction of endothelial dysfunction, promotion of vascular microcalcification, as well as stimulation of cell proliferation, autophagy, apoptosis, and death. S100A9 can serve as a biomarker for diagnosis, prediction, and evaluation of cardiovascular diseases, and it is also considered a potential therapeutic target.</description><subject>Advanced glycosylation end products</subject><subject>Aneurysms</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Blood vessels</subject><subject>Calcification</subject><subject>Calcification (ectopic)</subject><subject>Calgranulin B - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Leukocytes</subject><subject>Molecular modelling</subject><subject>Myeloid cells</subject><subject>Myocardial infarction</subject><subject>Myocarditis</subject><subject>Neutrophils</subject><subject>Oxidative Stress</subject><subject>Pathogenesis</subject><subject>Physiology</subject><subject>Preeclampsia</subject><subject>Proteins</subject><subject>Pulmonary hypertension</subject><subject>Review</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><issn>0960-7722</issn><issn>1365-2184</issn><issn>1365-2184</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</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>eNp1kU1LAzEQhoMoWqsH_4AseNHD2kw-d71IKX6BoPhxDtkka7dsd2vSrfTfm1oVFZzLwMzDwwwvQgeATyHWwMz8KVBBxQbqxc5TAhnbRD2cC5xKScgO2g1hgjFQkGIb7dCMY8Yk66GzoV3oxriQVE0yH7skzDu7TNoyeQSMh_lqbLS3VbvQwXS19omtgtPBhT20Veo6uP3P3kfPlxdPo-v09u7qZjS8TQ3DTKQWsASag9DCSS4YmKK0kvCCErAWoNCFZJkVwoHl2nLsROGMMFmZEWJzTvvofO2ddcXUWeOaude1mvlqqv1StbpSvzdNNVYv7UIBkJwxIqPh-NPg29fOhbmaVsG4utaNa7ugSC6JxJxyFtGjP-ik7XwT_1MUZxIzLGQWqZM1ZXwbgnfl9zWA1SoSFSNRH5FE9vDn-d_kVwYRGKyBt6p2y_9NanT_sFa-A3L8k-U</recordid><startdate>202408</startdate><enddate>202408</enddate><creator>Chen, Fengling</creator><creator>He, Ziyu</creator><creator>Wang, Chengming</creator><creator>Si, Jiajia</creator><creator>Chen, Zhu</creator><creator>Guo, Yuan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202408</creationdate><title>Advances in the study of S100A9 in cardiovascular diseases</title><author>Chen, Fengling ; He, Ziyu ; Wang, Chengming ; Si, Jiajia ; Chen, Zhu ; Guo, Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4046-d10713916a6e75641cbfd725b321dd11bab748d66e1d5ad50e6bec6c8f822d953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Advanced glycosylation end products</topic><topic>Aneurysms</topic><topic>Animals</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Blood vessels</topic><topic>Calcification</topic><topic>Calcification (ectopic)</topic><topic>Calgranulin B - metabolism</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular Diseases - metabolism</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Dendritic cells</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory response</topic><topic>Leukocytes</topic><topic>Molecular modelling</topic><topic>Myeloid cells</topic><topic>Myocardial infarction</topic><topic>Myocarditis</topic><topic>Neutrophils</topic><topic>Oxidative Stress</topic><topic>Pathogenesis</topic><topic>Physiology</topic><topic>Preeclampsia</topic><topic>Proteins</topic><topic>Pulmonary hypertension</topic><topic>Review</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Fengling</creatorcontrib><creatorcontrib>He, Ziyu</creatorcontrib><creatorcontrib>Wang, Chengming</creatorcontrib><creatorcontrib>Si, Jiajia</creatorcontrib><creatorcontrib>Chen, Zhu</creatorcontrib><creatorcontrib>Guo, Yuan</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</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>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>Cell proliferation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Fengling</au><au>He, Ziyu</au><au>Wang, Chengming</au><au>Si, Jiajia</au><au>Chen, Zhu</au><au>Guo, Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Advances in the study of S100A9 in cardiovascular diseases</atitle><jtitle>Cell proliferation</jtitle><addtitle>Cell Prolif</addtitle><date>2024-08</date><risdate>2024</risdate><volume>57</volume><issue>8</issue><spage>e13636</spage><epage>n/a</epage><pages>e13636-n/a</pages><issn>0960-7722</issn><issn>1365-2184</issn><eissn>1365-2184</eissn><abstract>Cardiovascular disease (CVD) is a group of diseases that primarily affect the heart or blood vessels, with high disability and mortality rates, posing a serious threat to human health. The causative factors, pathogenesis, and characteristics of common CVD differ, but they all involve common pathological processes such as inflammation, oxidative stress, and fibrosis. S100A9 belongs to the S100 family of calcium‐binding proteins, which are mainly secreted by myeloid cells and bind to the Toll‐like receptor 4 and receptor for advanced glycation end products and is involved in regulating pathological processes such as inflammatory response, fibrosis, vascular calcification, and endothelial barrier function in CVD. The latest research has found that S100A9 is a key biomarker for diagnosing and predicting various CVD. Therefore, this article reviews the latest research progress on the diagnostic and predictive, and therapeutic value of S100A9 in inflammatory‐related CVD such as atherosclerosis, myocardial infarction, and arterial aneurysm and summarizes its molecular mechanisms in the progression of CVD, aiming to explore new predictive methods and to identify potential intervention targets for CVD in clinical practice.
S100A9 is released by immune and tissue cells in response to stressors such as damage, inflammation, and oxidative stress. This leads to the amplification of inflammation, anti‐inflammatory effects, induction of endothelial dysfunction, promotion of vascular microcalcification, as well as stimulation of cell proliferation, autophagy, apoptosis, and death. S100A9 can serve as a biomarker for diagnosis, prediction, and evaluation of cardiovascular diseases, and it is also considered a potential therapeutic target.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38504474</pmid><doi>10.1111/cpr.13636</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Advanced glycosylation end products Aneurysms Animals Arteriosclerosis Atherosclerosis Biomarkers Biomarkers - metabolism Blood vessels Calcification Calcification (ectopic) Calgranulin B - metabolism Cardiomyocytes Cardiomyopathy Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - metabolism Chemokines Cytokines Dendritic cells Fibroblasts Fibrosis Heart attacks Heart diseases Humans Inflammation Inflammation - metabolism Inflammatory response Leukocytes Molecular modelling Myeloid cells Myocardial infarction Myocarditis Neutrophils Oxidative Stress Pathogenesis Physiology Preeclampsia Proteins Pulmonary hypertension Review TLR4 protein Toll-like receptors |
title | Advances in the study of S100A9 in cardiovascular diseases |
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