ArticleProceedings of the National Academy of Sciences of the United States of America2008
Requirement of protein kinase D1 for pathological cardiac remodeling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- Genome-wide association analysis and Mendelian randomization proteomics identify drug targets for heart failure.Nature communications · 2023Pooled it
- Article
- Tetralogy of Fallot and craniosynostosis - differential manifestation in a familial case of CHDED syndrome caused by novel pathogenic PRKD1 variant.Journal of human genetics · 2026Article
- Phosphorylation of CBX8 by PKD1 suppresses PRC1 activity and promotes cell senescence.Oncogene · 2026Article
- Internalized β2-Adrenergic Receptors Oppose PLC-Dependent Hypertrophic Signaling.Circulation research · 2024Article
- Effect of deletion of the protein kinase PRKD1 on development of the mouse embryonic heart.Journal of anatomy · 2024Article
- Protein Kinase D Plays a Crucial Role in Maintaining Cardiac Homeostasis by Regulating Post-Translational Modifications of Myofilament Proteins.International journal of molecular sciences · 2024Article
- Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3Frontiers in immunology · 2024Article
- Cardiac Protein Kinase D1 ablation alters the myocytes β-adrenergic response.Journal of molecular and cellular cardiology · 2023Article
- Loss of Protein Kinase D2 Activity Protects Against Bleomycin-Induced Dermal Fibrosis in Mice.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Protein kinase D1 (Prkd1) deletion in brown adipose tissue leads to altered myogenic gene expression after cold exposure, while thermogenesis remains intact.Physiological reports · 2023Article
- Small Molecule Inhibitors of Protein Kinase D: Early Development, Current Approaches, and Future Directions.Journal of medicinal chemistry · 2023Review
- Metabolic remodeling in cardiac hypertrophy and heart failure with reduced ejection fraction occurs independent of transcription factor EB in mice.Frontiers in cardiovascular medicine · 2023Article
- Protein Kinase D1 Regulates Cardiac Hypertrophy, Potassium Channel Remodeling, and Arrhythmias in Heart Failure.Journal of the American Heart Association · 2022Article
- The Transcription Factor EB (TFEB) Sensitizes the Heart to Chronic Pressure Overload.International journal of molecular sciences · 2022Article
- Angiotensin II Mediates Cardiomyocyte Hypertrophy in Atrial Cardiomyopathy via Epigenetic Transcriptional Regulation.Computational and mathematical methods in medicine · 2022Article
- Decoding the Cardiac Actions of Protein Kinase D Isoforms.Molecular pharmacology · 2021Review
- Pathogenic Mechanisms of Hypertrophic Cardiomyopathy beyond Sarcomere Dysfunction.International journal of molecular sciences · 2021Review
- Review
- Protein Kinase D2 drives chylomicron-mediated lipid transport in the intestine and promotes obesity.EMBO molecular medicine · 2021Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adult heart responds to biomechanical stress and neurohormonal signaling by hypertrophic growth, accompanied by fibrosis, diminished pump function, and activation of a fetal gene program. Class II histone deacetylases (HDACs) suppress stress-dependent remodeling of the heart via their association with the MEF2 transcription factor, an activator of heart disease. Protein kinase D (PKD) is a stress-responsive kinase that phosphorylates class II HDACs, resulting in their dissociation from MEF2 with consequent activation of MEF2 target genes. To test whether PKD1 is required for pathological cardiac remodeling in vivo, we generated mice with a conditional PKD1-null allele. Mice with cardiac-specific deletion of PKD1 were viable and showed diminished hypertrophy, fibrosis, and fetal gene activation as well as improved cardiac function in response to pressure overload or chronic adrenergic and angiotensin II signaling. We conclude that PKD1 functions as a key transducer of stress stimuli involved in pathological cardiac remodeling in vivo.
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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.