ArticleThe Journal of clinical investigation2006
Transcription factor MITF regulates cardiac growth and hypertrophy.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Effect of thyroid dysfunction on N-terminal pro-B-type natriuretic peptide levels: A systematic review and meta-analysis.Frontiers in endocrinology · 2023Pooled it
- Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure.Nature communications · 2022Pooled it
- Genomic analyses implicate noncoding de novo variants in congenital heart disease.Nature genetics · 2020Trial
- Spatially guided in vivo single-cell functional genomics of postnatal heart.Nature cardiovascular research · 2026Article
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- Single-nucleus RNA sequencing reveals the pathological process and key transcription factor of sorafenib-induced cardiotoxicity.BMC medicine · 2026Article
- Angiotensin-(1-7) Alleviates Isoproterenol-Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor.Acta physiologica (Oxford, England) · 2026Article
- Transcription factor MITF regulates masseter muscle growth and development.Physiological reports · 2025Article
- Single-cell transcriptomic profiling reveals cell type heterogeneity between HFpEF and HFrEF.Communications biology · 2025Article
- Large-scale genome-wide association analyses identify novel genetic loci and mechanisms in hypertrophic cardiomyopathy.Nature genetics · 2025Article
- Genome-wide association study reveals mechanisms underlying dilated cardiomyopathy and myocardial resilience.Nature genetics · 2024Article
- Review
- Leveraging chromatin state transitions for the identification of regulatory networks orchestrating heart regeneration.Nucleic acids research · 2024Article
- Article
- The C-terminal transactivation domain of MITF interacts promiscuously with co-activator CBP/p300.Scientific reports · 2023Article
- Genetic Determinants of the Interventricular Septum Are Linked to Ventricular Septal Defects and Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2023Article
- Genetic architecture of heart failure with preserved versus reduced ejection fraction.Nature communications · 2022Article
- Article
- PIWI-Interacting RNA HAAPIR Regulates Cardiomyocyte Death After Myocardial Infarction by Promoting NAT10-Mediated acAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Taiji-reprogram: a framework to uncover cell-type specific regulators and predict cellular reprogramming cocktails.NAR genomics and bioinformatics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High levels of microphthalmia transcription factor (MITF) expression have been described in several cell types, including melanocytes, mast cells, and osteoclasts. MITF plays a pivotal role in the regulation of specific genes in these cells. Although its mRNA has been found to be present in relatively high levels in the heart, its cardiac role has never been explored. Here we show that a specific heart isoform of MITF is expressed in cardiomyocytes and can be induced by beta-adrenergic stimulation but not by paired box gene 3 (PAX3), the regulator of the melanocyte MITF isoform. In 2 mouse strains with different MITF mutations, heart weight/body weight ratio was decreased as was the hypertrophic response to beta-adrenergic stimulation. These mice also demonstrated a tendency to sudden death following beta-adrenergic stimulation. Most impressively, 15-month-old MITF-mutated mice had greatly decreased heart weight/body weight ratio, systolic function, and cardiac output. In contrast with normal mice, in the MITF-mutated mice, beta-adrenergic stimulation failed to induce B-type natriuretic peptide (BNP), an important modulator of cardiac hypertrophy, while atrial natriuretic peptide levels and phosphorylated Akt were increased, suggesting a cardiac stress response. In addition, cardiomyocytes cultured with siRNA against MITF showed a substantial decrease in BNP promoter activity. Thus, for what we believe is the first time, we have demonstrated that MITF plays an essential role in beta-adrenergic-induced cardiac hypertrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.