ArticleSignal transduction and targeted therapy2024
DEAD-box helicase 17 (DDX17) protects cardiac function by promoting mitochondrial homeostasis in heart failure.
Article in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Tau Overexpression Causes Cardiac Hypertrophy by Disrupting Mitochondrial Homeostasis.International journal of molecular sciences · 2026Article
- Sirt5 preserves mitochondrial homeostasis to improve cardiac function in ischemia-reperfusion injury by inhibiting ANT2 lysine lactylation modification.Cellular and molecular life sciences : CMLS · 2026Article
- miR-125b Attenuates Sepsis-Induced Hippocampal Mitochondrial Fission and Cognitive Impairment via the ROS/p53 Pathway.Molecular neurobiology · 2026Article
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure.Journal of cardiovascular translational research · 2026Review
- DHX37 and tumor growth: a novel avenue for melanoma research.Journal of translational medicine · 2026Article
- DDX17-mediated raptor-dependent mTORC1 activation links autophagy inhibition and metabolic compensation in HCC development.Cellular & molecular biology letters · 2026Article
- Biallelic PAX7 variants cause a novel Satellite Cell-opathy with progressive muscle involvement resembling facioscapulohumeral muscular dystrophy.Cell death & disease · 2026Article
- Mechanisms of Protection Against Oxidative Stress During Hibernation.International journal of molecular sciences · 2026Review
- A defined multi-metabolite formulation derived from Salvia miltiorrhiza alleviates obesity-associated cardiac lipotoxicity via modulating mitochondrial dynamics.Frontiers in pharmacology · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism.Frontiers in immunology · 2026Article
- Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity.Frontiers in physiology · 2026Review
- [Silencing DDX17 inhibits proliferation and migration of pulmonary arterial smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Carfilzomib triggers cardiotoxicity by suppressing SENP1-mediated deSUMOylation of DDX17.Acta biochimica et biophysica Sinica · 2025Article
- The RNA helicase DDX17 enhances androgen receptor stability by interacting with the E3 ubiquitin ligase SPOP in prostate cancer.Translational andrology and urology · 2025Article
- Mitochondrial homeostasis restoring peptide-drug conjugates with ROS-responsive NO releasing ability for targeted therapy of myocardial infarction.Journal of nanobiotechnology · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
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Authors and funding
27 authors.
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Abstract
DEAD-box helicase 17 (DDX17) is a typical member of the DEAD-box family with transcriptional cofactor activity. Although DDX17 is abundantly expressed in the myocardium, its role in heart is not fully understood. We generated cardiomyocyte-specific Ddx17-knockout mice (Ddx17-cKO), cardiomyocyte-specific Ddx17 transgenic mice (Ddx17-Tg), and various models of cardiomyocyte injury and heart failure (HF). DDX17 is downregulated in the myocardium of mouse models of heart failure and cardiomyocyte injury. Cardiomyocyte-specific knockout of Ddx17 promotes autophagic flux blockage and cardiomyocyte apoptosis, leading to progressive cardiac dysfunction, maladaptive remodeling and progression to heart failure. Restoration of DDX17 expression in cardiomyocytes protects cardiac function under pathological conditions. Further studies showed that DDX17 can bind to the transcriptional repressor B-cell lymphoma 6 (BCL6) and inhibit the expression of dynamin-related protein 1 (DRP1). When DDX17 expression is reduced, transcriptional repression of BCL6 is attenuated, leading to increased DRP1 expression and mitochondrial fission, which in turn leads to impaired mitochondrial homeostasis and heart failure. We also investigated the correlation of DDX17 expression with cardiac function and DRP1 expression in myocardial biopsy samples from patients with heart failure. These findings suggest that DDX17 protects cardiac function by promoting mitochondrial homeostasis through the BCL6-DRP1 pathway in heart failure.
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