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The transcription factor Y-box binding protein 1 (YB-1) can interact with transcription factors involved in cardiac hypertrophy and may thereby interfere with the hypertrophy growth process. Therefore, the question arises as to whether YB-1 influences cardiomyocyte hypertrophy and might thereby influence the development of heart failure. YB-1 expression is downregulated in human heart biopsies of patients with ischemic cardiomyopathy (n = 8), leading to heart failure. To study the impact of reduced YB-1 in cardiac cells, we performed small interfering RNA (siRNA) experiments in H9C2 cells as well as in adult cardiomyocytes (CMs) of rats. The specificity of YB-1 siRNA was analyzed by a miRNA-like off-target prediction assay identifying potential genes. Testing three high-scoring genes by transfecting cardiac cells with YB-1 siRNA did not result in downregulation of these genes in contrast to YB-1, whose downregulation increased hypertrophic growth. Hypertrophic growth was mediated by PI3K under PE stimulation, as well by downregulation with YB-1 siRNA. On the other hand, overexpression of YB-1 in CMs, caused by infection with an adenovirus encoding YB-1 (AdYB-1), prevented hypertrophic growth under \u03b1-adrenergic stimulation with phenylephrine (PE), but not under stimulation with growth differentiation factor 15 (GDF15; n = 10\u201316). An adenovirus encoding the green fluorescent protein (AdGFP) served as the control. YB-1 overexpression enhanced the mRNA expression of the Gq inhibitor regulator of G-protein signaling 2 (RGS2) under PE stimulation (n = 6), potentially explaining its inhibitory effect on PE-induced hypertrophic growth. This study shows that YB-1 protects cardiomyocytes against PE-induced hypertrophic growth. Like in human end-stage heart failure, YB-1 downregulation may cause the heart to lose its protection against hypertrophic stimuli and progress to heart failure. Therefore, the transcription factor YB-1 is a pivotal signaling molecule, providing perspectives for therapeutic approaches.<\/jats:p>","DOI":"10.3390\/ijms25010401","type":"journal-article","created":{"date-parts":[[2023,12,28]],"date-time":"2023-12-28T03:30:34Z","timestamp":1703734234000},"page":"401","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["YB-1 Is a Novel Target for the Inhibition of \u03b1-Adrenergic-Induced Hypertrophy"],"prefix":"10.3390","volume":"25","author":[{"given":"Jacqueline","family":"Heger","sequence":"first","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Partsch","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Harjung","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2758-0784","authenticated-orcid":false,"given":"Zolt\u00e1n V.","family":"Varga","sequence":"additional","affiliation":[{"name":"HCEMM-SU Cardiometabolic Immunology Research Group, 1094 Budapest, Hungary"},{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1094 Budapest, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tam\u00e1s","family":"Baranyai","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1094 Budapest, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Wei\u00df","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea","family":"Kremer","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabian","family":"Locquet","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Przemyslaw","family":"Leszek","sequence":"additional","affiliation":[{"name":"Department of Heart Failure and Transplantology, Cardinal Stefan Wyszy\u0144ski Institute of Cardiology, 04-628 Warszawa, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6492-0426","authenticated-orcid":false,"given":"Bence","family":"\u00c1gg","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1094 Budapest, Hungary"},{"name":"Pharmahungary Group, 6722 Szeged, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0379-2181","authenticated-orcid":false,"given":"Bettina","family":"Benczik","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1094 Budapest, Hungary"},{"name":"Pharmahungary Group, 6722 Szeged, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P\u00e9ter","family":"Ferdinandy","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1094 Budapest, Hungary"},{"name":"Pharmahungary Group, 6722 Szeged, Hungary"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3017-0476","authenticated-orcid":false,"given":"Rainer","family":"Schulz","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9094-773X","authenticated-orcid":false,"given":"Gerhild","family":"Euler","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus Liebig University, 35392 Giessen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,12,28]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1007\/s00392-006-2005-z","article-title":"Pathophysiology of chronic heart failure","volume":"95","author":"Weil","year":"2006","journal-title":"Clin. 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