ArticleScientific reports2017
The valosin-containing protein is a novel mediator of mitochondrial respiration and cell survival in the heart in vivo.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Cardiomyopathy in valosin-containing protein multisystem proteinopathy: Evaluation, diagnosis, and management.American heart journal plus : cardiology research and practice · 2025Review
- Nonstructural Roles of Junctophilin-2 in the Heart.JACC. Basic to translational science · 2025Review
- A pathogenic mutation in the ALS/FTD gene VCP induces mitochondrial hypermetabolism by modulating the permeability transition pore.Acta neuropathologica communications · 2024Article
- Targeting calpain-2-mediated junctophilin-2 cleavage delays heart failure progression following myocardial infarction.Journal of molecular and cellular cardiology · 2024Article
- Cardiac-Specific Suppression of Valosin-Containing Protein Induces Progressive Heart Failure and Premature Mortality Correlating with Temporal Dysregulations in mTOR Complex 2 and Protein Phosphatase 1.International journal of molecular sciences · 2024Article
- Distinct features of the regenerating heart uncovered through comparative single-cell profiling.Biology open · 2024Article
- New Insights into Cardiovascular Diseases Treatment Based on Molecular Targets.International journal of molecular sciences · 2023Review
- Review
- DUSP1 interacts with and dephosphorylates VCP to improve mitochondrial quality control against endotoxemia-induced myocardial dysfunction.Cellular and molecular life sciences : CMLS · 2023Article
- Distinct features of the regenerating heart uncovered through comparative single-cell profiling.bioRxiv : the preprint server for biology · 2023Article
- CircRNA Samd4 induces cardiac repair after myocardial infarction by blocking mitochondria-derived ROS output.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Valosin Containing Protein as a Specific Biomarker for Predicting the Development of Acute Coronary Syndrome and Its Complication.Frontiers in cardiovascular medicine · 2022Article
- Article
- Structural and Functional Remodeling of Mitochondria in Cardiac Diseases.International journal of molecular sciences · 2021Review
- Emerging role of VCP/p97 in cardiovascular diseases: novel insights and therapeutic opportunities.Biochemical Society transactions · 2021Review
- Novel genomic targets of valosin-containing protein in protecting pathological cardiac hypertrophy.Scientific reports · 2020Article
- The Physiological and Pathological Roles of Mitochondrial Calcium Uptake in Heart.International journal of molecular sciences · 2020Review
- Valosin-Containing Protein, a Calcium-Associated ATPase Protein, in Endoplasmic Reticulum and Mitochondrial Function and Its Implications for Diseases.International journal of molecular sciences · 2020Review
- Partial Depletion of Peripheral M1 Macrophages Reverses Motor Deficits in MPTP-Treated Mouse by Suppressing Neuroinflammation and Dopaminergic Neurodegeneration.Frontiers in aging neuroscience · 2018Article
- VCP represses pathological cardiac hypertrophy.Aging · 2017Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The valosin-containing protein (VCP) participates in signaling pathways essential for cell homeostasis in multiple tissues, however, its function in the heart in vivo remains unknown. Here we offer the first description of the expression, function and mechanism of action of VCP in the mammalian heart in vivo in both normal and stress conditions. By using a transgenic (TG) mouse with cardiac-specific overexpression (3.5-fold) of VCP, we demonstrate that VCP is a new and powerful mediator of cardiac protection against cell death in vivo, as evidenced by a 50% reduction of infarct size after ischemia/reperfusion versus wild type. We also identify a novel role of VCP in preserving mitochondrial respiration and in preventing the opening of mitochondrial permeability transition pore in cardiac myocytes under stress. In particular, by genetic deletion of inducible isoform of nitric oxide synthase (iNOS) from VCP TG mouse and by pharmacological inhibition of iNOS in isolated cardiac myocytes, we reveal that an increase of expression and activity of iNOS in cardiomyocytes by VCP is an essential mechanistic link of VCP-mediated preservation of mitochondrial function. These data together demonstrate that VCP may represent a novel therapeutic avenue for the prevention of myocardial ischemia.
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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.