ArticleAging cell2017
The valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- FTO-Eci1 Axis Mediates Exercise-Induced Cardioprotection in Pressure Overload Mice.Biomolecules · 2026Article
- Cardiomyopathy in valosin-containing protein multisystem proteinopathy: Evaluation, diagnosis, and management.American heart journal plus : cardiology research and practice · 2025Review
- 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
- Article
- CRISPR/Cas9-Mediated Constitutive Loss of VCP (Valosin-Containing Protein) Impairs Proteostasis and Leads to Defective Striated Muscle Structure and Function In Vivo.International journal of molecular sciences · 2022Article
- Article
- Hsp22 Deficiency Induces Age-Dependent Cardiac Dilation and Dysfunction by Impairing Autophagy, Metabolism, and Oxidative Response.Antioxidants (Basel, Switzerland) · 2021Article
- Neuronal VCP loss of function recapitulates FTLD-TDP pathology.Cell reports · 2021Article
- Vascular Stress Signaling in Hypertension.Circulation research · 2021Review
- Emerging role of VCP/p97 in cardiovascular diseases: novel insights and therapeutic opportunities.Biochemical Society transactions · 2021Review
- Exosomes Released from CaSR-Stimulated PMNs Reduce Ischaemia/Reperfusion Injury.Oxidative medicine and cellular longevity · 2021Article
- 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
- Disruption of valosin-containing protein activity causes cardiomyopathy and reveals pleiotropic functions in cardiac homeostasis.The Journal of biological chemistry · 2019Article
- Heat-shock transcription factor 1 is critically involved in the ischaemia-induced cardiac hypertrophy via JAK2/STAT3 pathway.Journal of cellular and molecular medicine · 2018Article
- New Insights Into the Role of mTOR Signaling in the Cardiovascular System.Circulation research · 2018Review
- VCP represses pathological cardiac hypertrophy.Aging · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Hypertension-induced left ventricular hypertrophy (LVH) is an independent risk factor for heart failure. Regression of LVH has emerged as a major goal in the treatment of hypertensive patients. Here, we tested our hypothesis that the valosin-containing protein (VCP), an ATPase associate protein, is a novel repressor of cardiomyocyte hypertrophy under the pressure overload stress. Left ventricular hypertrophy (LVH) was determined by echocardiography in 4-month male spontaneously hypertensive rats (SHRs) vs. age-matched normotensive Wistar Kyoto (WKY) rats. VCP expression was found to be significantly downregulated in the left ventricle (LV) tissues from SHRs vs. WKY rats. Pressure overload was induced by transverse aortic constriction (TAC) in wild-type (WT) mice. At the end of 2 weeks, mice with TAC developed significant LVH whereas the cardiac function remained unchanged. A significant reduction of VCP at both the mRNA and protein levels in hypertrophic LV tissue was found in TAC WT mice compared to sham controls. Valosin-containing protein VCP expression was also observed to be time- and dose-dependently reduced in vitro in isolated neonatal rat cardiomyocytes upon the treatment of angiotensin II. Conversely, transgenic (TG) mice with cardiac-specific overexpression of VCP showed a significant repression in TAC-induced LVH vs. litter-matched WT controls upon 2-week TAC. TAC-induced activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling observed in WT mice LVs was also significantly blunted in VCP TG mice. In conclusion, VCP acts as a novel repressor that is able to prevent cardiomyocyte hypertrophy from pressure overload by modulating the mTORC1 signaling pathway.
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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.