Genetic Association of Beta-Myosin Heavy-Chain Gene (MYH7) with Cardiac Dysfunction
Cardiac dysfunction accelerates the risk of heart failure, and its pathogenesis involves a complex interaction between genetic and environmental factors. Variations in myosin affect contractile abilities of cardiomyocytes and cause structural and functional abnormalities in myocardium. The study aim...
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| Veröffentlicht in: | Genes 2022-08, Vol.13 (9), p.1554 |
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| creator | Yousaf, Memoona Khan, Waqas Ahmed Shahzad, Khurrum Khan, Haq Nawaz Ali, Basharat Hussain, Misbah Awan, Fazli Rabbi Mustafa, Hamid Sheikh, Farah Nadia |
| description | Cardiac dysfunction accelerates the risk of heart failure, and its pathogenesis involves a complex interaction between genetic and environmental factors. Variations in myosin affect contractile abilities of cardiomyocytes and cause structural and functional abnormalities in myocardium. The study aims to find the association of MYH7 rs121913642 (c.1594 T>C) and rs121913645 (c.667G>A) variants with cardiac dysfunction in the Punjabi Pakistani population. Patients with heart failure (n = 232) and healthy controls (n = 205) were enrolled in this study. MYH7 variant genotyping was performed using tetra ARMS-PCR. MYH7 rs121913642 TC genotype was significantly more prevalent in the patient group (p < 0.001). However, MYH7 rs121913645 genotype frequencies were not significantly different between the patient and control groups (p < 0.666). Regression analysis also revealed that the rs121913642 C allele increases the risk of cardiac failure by ~2 [OR:1.98, CI: 1.31−2.98, p < 0.001] in comparison to the T allele. High levels of the cardiac enzymes cardiac troponin I (cTnI) and CK-MB were observed in patients. There was also an increase in total cholesterol, LDL cholesterol, and uric acid in patients compared to the healthy control group (p < 0.001). In conclusion, the MYH7 gene variant rs121913642 is genetically associated with cardiac dysfunction and involved in the pathogenesis of HF. |
| doi_str_mv | 10.3390/genes13091554 |
| format | Article |
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Variations in myosin affect contractile abilities of cardiomyocytes and cause structural and functional abnormalities in myocardium. The study aims to find the association of MYH7 rs121913642 (c.1594 T>C) and rs121913645 (c.667G>A) variants with cardiac dysfunction in the Punjabi Pakistani population. Patients with heart failure (n = 232) and healthy controls (n = 205) were enrolled in this study. MYH7 variant genotyping was performed using tetra ARMS-PCR. MYH7 rs121913642 TC genotype was significantly more prevalent in the patient group (p < 0.001). However, MYH7 rs121913645 genotype frequencies were not significantly different between the patient and control groups (p < 0.666). Regression analysis also revealed that the rs121913642 C allele increases the risk of cardiac failure by ~2 [OR:1.98, CI: 1.31−2.98, p < 0.001] in comparison to the T allele. High levels of the cardiac enzymes cardiac troponin I (cTnI) and CK-MB were observed in patients. There was also an increase in total cholesterol, LDL cholesterol, and uric acid in patients compared to the healthy control group (p < 0.001). In conclusion, the MYH7 gene variant rs121913642 is genetically associated with cardiac dysfunction and involved in the pathogenesis of HF.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes13091554</identifier><identifier>PMID: 36140722</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alleles ; Calcium-binding protein ; Cardiac Myosins - genetics ; Cardiomyocytes ; Cardiomyopathy ; Cholesterol ; Cholesterol, LDL - genetics ; Congestive heart failure ; Creatinine ; Development and progression ; Ejection fraction ; Environmental factors ; Genetic aspects ; Genetic diversity ; Genomes ; Genotype & phenotype ; Genotypes ; Genotyping ; Health aspects ; Heart Diseases ; Heart failure ; Heart Failure - genetics ; High density lipoprotein ; Humans ; Kinases ; Laboratories ; Low density lipoprotein ; Muscle contraction ; Mutation ; MYH7 gene ; Myocardium ; Myosin ; Myosin Heavy Chains - genetics ; Pathogenesis ; Patients ; Phenotype ; Proteins ; Structure-function relationships ; Troponin ; Troponin I ; Troponin I - genetics ; Uric Acid ; Ventricular Myosins - genetics</subject><ispartof>Genes, 2022-08, Vol.13 (9), p.1554</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-c482t-87496774797e80f47ec8655632e0bc5ed832486abba9cffc14055578cdfdfc903</citedby><cites>FETCH-LOGICAL-c482t-87496774797e80f47ec8655632e0bc5ed832486abba9cffc14055578cdfdfc903</cites><orcidid>0000-0003-1279-420X</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/PMC9498774/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9498774/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36140722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yousaf, Memoona</creatorcontrib><creatorcontrib>Khan, Waqas Ahmed</creatorcontrib><creatorcontrib>Shahzad, Khurrum</creatorcontrib><creatorcontrib>Khan, Haq Nawaz</creatorcontrib><creatorcontrib>Ali, Basharat</creatorcontrib><creatorcontrib>Hussain, Misbah</creatorcontrib><creatorcontrib>Awan, Fazli Rabbi</creatorcontrib><creatorcontrib>Mustafa, Hamid</creatorcontrib><creatorcontrib>Sheikh, Farah Nadia</creatorcontrib><title>Genetic Association of Beta-Myosin Heavy-Chain Gene (MYH7) with Cardiac Dysfunction</title><title>Genes</title><addtitle>Genes (Basel)</addtitle><description>Cardiac dysfunction accelerates the risk of heart failure, and its pathogenesis involves a complex interaction between genetic and environmental factors. Variations in myosin affect contractile abilities of cardiomyocytes and cause structural and functional abnormalities in myocardium. The study aims to find the association of MYH7 rs121913642 (c.1594 T>C) and rs121913645 (c.667G>A) variants with cardiac dysfunction in the Punjabi Pakistani population. Patients with heart failure (n = 232) and healthy controls (n = 205) were enrolled in this study. MYH7 variant genotyping was performed using tetra ARMS-PCR. MYH7 rs121913642 TC genotype was significantly more prevalent in the patient group (p < 0.001). However, MYH7 rs121913645 genotype frequencies were not significantly different between the patient and control groups (p < 0.666). Regression analysis also revealed that the rs121913642 C allele increases the risk of cardiac failure by ~2 [OR:1.98, CI: 1.31−2.98, p < 0.001] in comparison to the T allele. High levels of the cardiac enzymes cardiac troponin I (cTnI) and CK-MB were observed in patients. There was also an increase in total cholesterol, LDL cholesterol, and uric acid in patients compared to the healthy control group (p < 0.001). In conclusion, the MYH7 gene variant rs121913642 is genetically associated with cardiac dysfunction and involved in the pathogenesis of HF.</description><subject>Alleles</subject><subject>Calcium-binding protein</subject><subject>Cardiac Myosins - genetics</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cholesterol</subject><subject>Cholesterol, LDL - genetics</subject><subject>Congestive heart failure</subject><subject>Creatinine</subject><subject>Development and progression</subject><subject>Ejection fraction</subject><subject>Environmental factors</subject><subject>Genetic aspects</subject><subject>Genetic diversity</subject><subject>Genomes</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Genotyping</subject><subject>Health aspects</subject><subject>Heart Diseases</subject><subject>Heart failure</subject><subject>Heart Failure - genetics</subject><subject>High density lipoprotein</subject><subject>Humans</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Low density lipoprotein</subject><subject>Muscle contraction</subject><subject>Mutation</subject><subject>MYH7 gene</subject><subject>Myocardium</subject><subject>Myosin</subject><subject>Myosin Heavy Chains - genetics</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Phenotype</subject><subject>Proteins</subject><subject>Structure-function relationships</subject><subject>Troponin</subject><subject>Troponin I</subject><subject>Troponin I - genetics</subject><subject>Uric Acid</subject><subject>Ventricular Myosins - genetics</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><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>eNptkUtPAyEUhYnRWFO7dGsmcaOLqQyPATYmtT5q0saFunBFKAMtpgUdpjX999JYq02EBTfwnXMPuQCcFLCLsYCXE-NNLDAUBaVkDxwhyHBOCKL7f-oW6MT4BtMiEEFID0ELlwWBDKEj8HSfLBqns16MQTvVuOCzYLNr06h8tArR-Wxg1HKV96cq1Ws8Ox-9DthF9umaadZXdeWUzm5W0S68XuuPwYFVs2g6m7MNXu5un_uDfPh4_9DvDXNNOGpyzogoGSNMMMOhJcxoXlJaYmTgWFNTcYwIL9V4rIS2VqfIlFLGdWUrqwXEbXD17fu-GM9NpY1vajWT77Wbq3olg3Jy98W7qZyEpRRE8NQ4GZxtDOrwsTCxkW9hUfuUWSJWlJTAohS_1ETNjHTehmSm5y5q2WOEMoRLThPV_YdKuzJzp4M31qX7HUH-LdB1iLE2dhu8gHI9Xbkz3cSf_v3tlv6ZJf4CEAuePQ</recordid><startdate>20220829</startdate><enddate>20220829</enddate><creator>Yousaf, Memoona</creator><creator>Khan, Waqas Ahmed</creator><creator>Shahzad, Khurrum</creator><creator>Khan, Haq Nawaz</creator><creator>Ali, Basharat</creator><creator>Hussain, Misbah</creator><creator>Awan, Fazli Rabbi</creator><creator>Mustafa, Hamid</creator><creator>Sheikh, Farah Nadia</creator><general>MDPI AG</general><general>MDPI</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>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>5PM</scope><orcidid>https://orcid.org/0000-0003-1279-420X</orcidid></search><sort><creationdate>20220829</creationdate><title>Genetic Association of Beta-Myosin Heavy-Chain Gene (MYH7) with Cardiac Dysfunction</title><author>Yousaf, Memoona ; 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Variations in myosin affect contractile abilities of cardiomyocytes and cause structural and functional abnormalities in myocardium. The study aims to find the association of MYH7 rs121913642 (c.1594 T>C) and rs121913645 (c.667G>A) variants with cardiac dysfunction in the Punjabi Pakistani population. Patients with heart failure (n = 232) and healthy controls (n = 205) were enrolled in this study. MYH7 variant genotyping was performed using tetra ARMS-PCR. MYH7 rs121913642 TC genotype was significantly more prevalent in the patient group (p < 0.001). However, MYH7 rs121913645 genotype frequencies were not significantly different between the patient and control groups (p < 0.666). Regression analysis also revealed that the rs121913642 C allele increases the risk of cardiac failure by ~2 [OR:1.98, CI: 1.31−2.98, p < 0.001] in comparison to the T allele. High levels of the cardiac enzymes cardiac troponin I (cTnI) and CK-MB were observed in patients. There was also an increase in total cholesterol, LDL cholesterol, and uric acid in patients compared to the healthy control group (p < 0.001). In conclusion, the MYH7 gene variant rs121913642 is genetically associated with cardiac dysfunction and involved in the pathogenesis of HF.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36140722</pmid><doi>10.3390/genes13091554</doi><orcidid>https://orcid.org/0000-0003-1279-420X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alleles Calcium-binding protein Cardiac Myosins - genetics Cardiomyocytes Cardiomyopathy Cholesterol Cholesterol, LDL - genetics Congestive heart failure Creatinine Development and progression Ejection fraction Environmental factors Genetic aspects Genetic diversity Genomes Genotype & phenotype Genotypes Genotyping Health aspects Heart Diseases Heart failure Heart Failure - genetics High density lipoprotein Humans Kinases Laboratories Low density lipoprotein Muscle contraction Mutation MYH7 gene Myocardium Myosin Myosin Heavy Chains - genetics Pathogenesis Patients Phenotype Proteins Structure-function relationships Troponin Troponin I Troponin I - genetics Uric Acid Ventricular Myosins - genetics |
| title | Genetic Association of Beta-Myosin Heavy-Chain Gene (MYH7) with Cardiac Dysfunction |
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