Vasovagal Syncope Is Associated with Variants in Genes Involved in Neurohumoral Signaling Pathways
Vasovagal syncope (VVS) is the most common cause of sudden loss of consciousness. VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic suscepti...
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| Veröffentlicht in: | Genes 2022-09, Vol.13 (9), p.1653 |
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| creator | Titov, Boris Matveeva, Natalya Kulakova, Olga Baulina, Natalia Bazyleva, Elizaveta Kheymets, Grigory Rogoza, Anatolii Pevzner, Alexander Favorova, Olga |
| description | Vasovagal syncope (VVS) is the most common cause of sudden loss of consciousness. VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic susceptibility. Since abnormal neurohumoral regulation plays an important role in VVS development, we analyzed the association of VVS with polymorphic variants of ADRA1A, ADRB1, HTR1A, ADORA2A, COMT, and NOS3 genes, the products of which are involved in neurohumoral signaling, in patients with a confirmed VVS diagnosis (157 subjects) and individuals without a history of syncope (161 subjects). We were able to identify the associations between VVS and alleles/genotypes ADRA1A rs1048101, ADRB1 rs1801253, ADORA2A rs5751876, and COMT rs4680, as well as NOS3 rs2070744 in biallelic combination with COMT rs4680. Thus, we are the first to observe, within a single study, the role of the genes that encode α- and β-adrenergic receptors, catechol-O-methyltransferase, adenosine receptors and nitric oxide synthase in VVS development. These findings demonstrate that the genes involved in neurohumoral signaling pathways contribute to the formation of a genetic susceptibility to VVS. |
| doi_str_mv | 10.3390/genes13091653 |
| format | Article |
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VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic susceptibility. Since abnormal neurohumoral regulation plays an important role in VVS development, we analyzed the association of VVS with polymorphic variants of ADRA1A, ADRB1, HTR1A, ADORA2A, COMT, and NOS3 genes, the products of which are involved in neurohumoral signaling, in patients with a confirmed VVS diagnosis (157 subjects) and individuals without a history of syncope (161 subjects). We were able to identify the associations between VVS and alleles/genotypes ADRA1A rs1048101, ADRB1 rs1801253, ADORA2A rs5751876, and COMT rs4680, as well as NOS3 rs2070744 in biallelic combination with COMT rs4680. Thus, we are the first to observe, within a single study, the role of the genes that encode α- and β-adrenergic receptors, catechol-O-methyltransferase, adenosine receptors and nitric oxide synthase in VVS development. These findings demonstrate that the genes involved in neurohumoral signaling pathways contribute to the formation of a genetic susceptibility to VVS.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes13091653</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Adenosine receptors ; Adrenergic receptors ; Age ; Autonomic nervous system ; Blood circulation ; Catechol ; Catechol O-methyltransferase ; Cerebral blood flow ; Disease ; Disease susceptibility ; Fainting ; Genetic aspects ; Genotype & phenotype ; Genotypes ; Health risk assessment ; Hypotension ; Hypothesis testing ; Methyltransferase ; Nitric-oxide synthase ; Physiological aspects ; Signal transduction ; Vasovagal syncope</subject><ispartof>Genes, 2022-09, Vol.13 (9), p.1653</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><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/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-dd4f4eb4cb6ab5a01187e09ecae75a6183a5f2c234fa8a984efc3e792946d17a3</citedby><cites>FETCH-LOGICAL-c389t-dd4f4eb4cb6ab5a01187e09ecae75a6183a5f2c234fa8a984efc3e792946d17a3</cites><orcidid>0000-0002-4369-2882 ; 0000-0002-5271-6698 ; 0000-0001-9967-2656 ; 0000-0002-2585-8471 ; 0000-0001-8767-2958</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/PMC9498630/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9498630/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Titov, Boris</creatorcontrib><creatorcontrib>Matveeva, Natalya</creatorcontrib><creatorcontrib>Kulakova, Olga</creatorcontrib><creatorcontrib>Baulina, Natalia</creatorcontrib><creatorcontrib>Bazyleva, Elizaveta</creatorcontrib><creatorcontrib>Kheymets, Grigory</creatorcontrib><creatorcontrib>Rogoza, Anatolii</creatorcontrib><creatorcontrib>Pevzner, Alexander</creatorcontrib><creatorcontrib>Favorova, Olga</creatorcontrib><title>Vasovagal Syncope Is Associated with Variants in Genes Involved in Neurohumoral Signaling Pathways</title><title>Genes</title><description>Vasovagal syncope (VVS) is the most common cause of sudden loss of consciousness. VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic susceptibility. Since abnormal neurohumoral regulation plays an important role in VVS development, we analyzed the association of VVS with polymorphic variants of ADRA1A, ADRB1, HTR1A, ADORA2A, COMT, and NOS3 genes, the products of which are involved in neurohumoral signaling, in patients with a confirmed VVS diagnosis (157 subjects) and individuals without a history of syncope (161 subjects). We were able to identify the associations between VVS and alleles/genotypes ADRA1A rs1048101, ADRB1 rs1801253, ADORA2A rs5751876, and COMT rs4680, as well as NOS3 rs2070744 in biallelic combination with COMT rs4680. Thus, we are the first to observe, within a single study, the role of the genes that encode α- and β-adrenergic receptors, catechol-O-methyltransferase, adenosine receptors and nitric oxide synthase in VVS development. These findings demonstrate that the genes involved in neurohumoral signaling pathways contribute to the formation of a genetic susceptibility to VVS.</description><subject>Adenosine receptors</subject><subject>Adrenergic receptors</subject><subject>Age</subject><subject>Autonomic nervous system</subject><subject>Blood circulation</subject><subject>Catechol</subject><subject>Catechol O-methyltransferase</subject><subject>Cerebral blood flow</subject><subject>Disease</subject><subject>Disease susceptibility</subject><subject>Fainting</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Health risk assessment</subject><subject>Hypotension</subject><subject>Hypothesis testing</subject><subject>Methyltransferase</subject><subject>Nitric-oxide synthase</subject><subject>Physiological aspects</subject><subject>Signal transduction</subject><subject>Vasovagal syncope</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptksFq3DAQhk1poSHJsXdBL7k4lSzZsi6FJaTpQmgLaXMVY3nsVbCljWRv2LePnIS2G6I5SMx8849mmCz7xOg554p-6dFhZJwqVpX8XXZUUMlzIYry_X_vj9lpjHc0HUELSsujrLmF6HfQw0Bu9s74LZJ1JKsYvbEwYUse7LQhtxAsuCkS68jVUois3c4PuxRPnh84B7-ZRx8WFds7GKzryS-YNg-wjyfZhw6GiKcv93H259vl74vv-fXPq_XF6jo3vFZT3raiE9gI01TQlEAZqyVShQZQllCxmkPZFabgooMaVC2wMxylKpSoWiaBH2dfn3W3czNia9BN6UN6G-wIYa89WH0YcXaje7_TSqi64jQJnL0IBH8_Y5z0aKPBYQCHfo66kExWtZKqTujnV-idn0Nq_ImqSkGZVP-oNF7U1nU-1TWLqF5JUcqCM7FQ529QyVocrfEOO5v8Bwn5c4IJPsaA3d8eGdXLMuiDZeCPO82oqw</recordid><startdate>20220915</startdate><enddate>20220915</enddate><creator>Titov, Boris</creator><creator>Matveeva, Natalya</creator><creator>Kulakova, Olga</creator><creator>Baulina, Natalia</creator><creator>Bazyleva, Elizaveta</creator><creator>Kheymets, Grigory</creator><creator>Rogoza, Anatolii</creator><creator>Pevzner, Alexander</creator><creator>Favorova, Olga</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</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>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>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4369-2882</orcidid><orcidid>https://orcid.org/0000-0002-5271-6698</orcidid><orcidid>https://orcid.org/0000-0001-9967-2656</orcidid><orcidid>https://orcid.org/0000-0002-2585-8471</orcidid><orcidid>https://orcid.org/0000-0001-8767-2958</orcidid></search><sort><creationdate>20220915</creationdate><title>Vasovagal Syncope Is Associated with Variants in Genes Involved in Neurohumoral Signaling Pathways</title><author>Titov, Boris ; Matveeva, Natalya ; Kulakova, Olga ; Baulina, Natalia ; Bazyleva, Elizaveta ; Kheymets, Grigory ; Rogoza, Anatolii ; Pevzner, Alexander ; Favorova, Olga</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-dd4f4eb4cb6ab5a01187e09ecae75a6183a5f2c234fa8a984efc3e792946d17a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenosine receptors</topic><topic>Adrenergic receptors</topic><topic>Age</topic><topic>Autonomic nervous system</topic><topic>Blood circulation</topic><topic>Catechol</topic><topic>Catechol O-methyltransferase</topic><topic>Cerebral blood flow</topic><topic>Disease</topic><topic>Disease susceptibility</topic><topic>Fainting</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Health risk assessment</topic><topic>Hypotension</topic><topic>Hypothesis testing</topic><topic>Methyltransferase</topic><topic>Nitric-oxide synthase</topic><topic>Physiological aspects</topic><topic>Signal transduction</topic><topic>Vasovagal syncope</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Titov, Boris</creatorcontrib><creatorcontrib>Matveeva, Natalya</creatorcontrib><creatorcontrib>Kulakova, Olga</creatorcontrib><creatorcontrib>Baulina, Natalia</creatorcontrib><creatorcontrib>Bazyleva, Elizaveta</creatorcontrib><creatorcontrib>Kheymets, Grigory</creatorcontrib><creatorcontrib>Rogoza, Anatolii</creatorcontrib><creatorcontrib>Pevzner, Alexander</creatorcontrib><creatorcontrib>Favorova, Olga</creatorcontrib><collection>CrossRef</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 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>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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Titov, Boris</au><au>Matveeva, Natalya</au><au>Kulakova, Olga</au><au>Baulina, Natalia</au><au>Bazyleva, Elizaveta</au><au>Kheymets, Grigory</au><au>Rogoza, Anatolii</au><au>Pevzner, Alexander</au><au>Favorova, Olga</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vasovagal Syncope Is Associated with Variants in Genes Involved in Neurohumoral Signaling Pathways</atitle><jtitle>Genes</jtitle><date>2022-09-15</date><risdate>2022</risdate><volume>13</volume><issue>9</issue><spage>1653</spage><pages>1653-</pages><issn>2073-4425</issn><eissn>2073-4425</eissn><abstract>Vasovagal syncope (VVS) is the most common cause of sudden loss of consciousness. VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic susceptibility. Since abnormal neurohumoral regulation plays an important role in VVS development, we analyzed the association of VVS with polymorphic variants of ADRA1A, ADRB1, HTR1A, ADORA2A, COMT, and NOS3 genes, the products of which are involved in neurohumoral signaling, in patients with a confirmed VVS diagnosis (157 subjects) and individuals without a history of syncope (161 subjects). We were able to identify the associations between VVS and alleles/genotypes ADRA1A rs1048101, ADRB1 rs1801253, ADORA2A rs5751876, and COMT rs4680, as well as NOS3 rs2070744 in biallelic combination with COMT rs4680. Thus, we are the first to observe, within a single study, the role of the genes that encode α- and β-adrenergic receptors, catechol-O-methyltransferase, adenosine receptors and nitric oxide synthase in VVS development. These findings demonstrate that the genes involved in neurohumoral signaling pathways contribute to the formation of a genetic susceptibility to VVS.</abstract><cop>Basel</cop><pub>MDPI AG</pub><doi>10.3390/genes13091653</doi><orcidid>https://orcid.org/0000-0002-4369-2882</orcidid><orcidid>https://orcid.org/0000-0002-5271-6698</orcidid><orcidid>https://orcid.org/0000-0001-9967-2656</orcidid><orcidid>https://orcid.org/0000-0002-2585-8471</orcidid><orcidid>https://orcid.org/0000-0001-8767-2958</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine receptors Adrenergic receptors Age Autonomic nervous system Blood circulation Catechol Catechol O-methyltransferase Cerebral blood flow Disease Disease susceptibility Fainting Genetic aspects Genotype & phenotype Genotypes Health risk assessment Hypotension Hypothesis testing Methyltransferase Nitric-oxide synthase Physiological aspects Signal transduction Vasovagal syncope |
| title | Vasovagal Syncope Is Associated with Variants in Genes Involved in Neurohumoral Signaling Pathways |
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