{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:41:52Z","timestamp":1787319712994,"version":"build-2736575974"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,2,24]],"date-time":"2022-02-24T00:00:00Z","timestamp":1645660800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Cardiomyopathies are a heterogeneous group of heart diseases that can gradually cause severe heart failure. In particular, dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) are the two main types of cardiomyopathies, yet the independent and communal biological mechanisms of both remain far from elucidated. Meanwhile, ferroptosis is a non-apoptotic form of cell death that has been proven to be associated with cardiomyopathies, but the concrete nature of the interaction remains unclear. Hence, this study explored the pathogenesis and ferroptosis mechanism of HCM and DCM\n                      <jats:italic>via<\/jats:italic>\n                      a bioinformatics analysis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Six datasets were downloaded from the Gene Expression Omnibus (GEO) database based on the study inclusion\/exclusion criteria. After screening the differentially expressed genes (DEGs) and hub genes of HCM and DCM, subsequent analyses, including functional annotation, co-expression, validation, and transcription factors (TF)\u2013mRNA\u2013microRNA (miRNA) regulatory network construction, were performed. In addition, ferroptosis-related DEGs were also identified and verified in HCM and DCM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found 171 independent DEGs of HCM mainly enriched in the regulation of ERK1 and ERK2 cascade, while 171 independent DEGs of DCM were significantly involved in cell adhesion. Meanwhile, 32 communal DEGs (26 upregulated genes and 6 downregulated genes) and 3 hub genes [periostin (\n                      <jats:italic>POSTN<\/jats:italic>\n                      ), insulin-like growth factor-binding protein-5 (\n                      <jats:italic>IGFBP5<\/jats:italic>\n                      ), and fibromodulin (\n                      <jats:italic>FMOD<\/jats:italic>\n                      )] were determined to be shared between HCM and DCM and the functional annotation of these genes highlighted the important position of growth hormone in HCM and DCM. Moreover, we identified activating transcription factor 3 (\n                      <jats:italic>ATF3<\/jats:italic>\n                      ), lysophosphatidylcholine acyltransferase 3 (\n                      <jats:italic>LPCAT3<\/jats:italic>\n                      ), and solute carrier family 1 member 5 (\n                      <jats:italic>SLC1A5<\/jats:italic>\n                      ) as ferroptosis-related genes in HCM and\n                      <jats:italic>STAT3<\/jats:italic>\n                      as a ferroptosis-related gene in DCM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The identified independent and communal DEGs contribute to uncover a potentially distinct and common mechanism of HCM and DCM and ferroptosis-related genes could provide us with a novel direction for exploration. In addition, 3 hub genes could be potential biomarkers or therapeutic targets in patients with cardiomyopathy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2022.824756","type":"journal-article","created":{"date-parts":[[2022,2,24]],"date-time":"2022-02-24T01:46:30Z","timestamp":1645667190000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":26,"title":["Exploring the Communal Pathogenesis, Ferroptosis Mechanism, and Potential Therapeutic Targets of Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy via a Microarray Data Analysis"],"prefix":"10.3389","volume":"9","author":[{"given":"Zuoxiang","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingyue","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenxing","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingqiang","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunjuan","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingyang","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weixiang","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tingbo","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,2,24]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1807","DOI":"10.1161\/CIRCULATIONAHA.106.174287","article-title":"Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention","volume":"113","author":"Maron","year":"2006","journal-title":"Circulation."},{"key":"B2","doi-asserted-by":"publisher","first-page":"7722","DOI":"10.3390\/ijms22147722","article-title":"Cardiomyopathies: an overview","volume":"22","author":"Ciarambino","year":"2021","journal-title":"Int J Mol Sci."},{"key":"B3","doi-asserted-by":"publisher","first-page":"1185","DOI":"10.1093\/eurjhf\/hfr074","article-title":"Novel correlations between the genotype and the phenotype of hypertrophic and dilated cardiomyopathy: results from the German Competence Network Heart Failure","volume":"13","author":"Waldmuller","year":"2011","journal-title":"Eur J Heart Fail."},{"key":"B4","doi-asserted-by":"publisher","first-page":"752","DOI":"10.1016\/s0140-6736(09)62023-7","article-title":"Dilated cardiomyopathy","volume":"375","author":"Jefferies","year":"2010","journal-title":"Lancet."},{"key":"B5","doi-asserted-by":"publisher","first-page":"201","DOI":"10.1016\/j.jacc.2009.02.075","article-title":"Diagnostic, prognostic, and therapeutic implications of genetic testing for hypertrophic cardiomyopathy","volume":"54","author":"Bos","year":"2009","journal-title":"J Am Coll Cardiol."},{"key":"B6","doi-asserted-by":"publisher","first-page":"785","DOI":"10.1161\/01.cir.92.4.785","article-title":"Prevalence of hypertrophic cardiomyopathy in a general population of young adults. echocardiographic analysis of 4111 subjects in the CARDIA Study. 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