ArticleCardiovascular research2013
The valosin-containing protein promotes cardiac survival through the inducible isoform of nitric oxide synthase.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Dual-pathway model of IL-6 and HSP22/HSP27 dynamics predicts post-PCI MACE in STEMI patients.BMC cardiovascular disorders · 2025Article
- Cardiomyopathy in valosin-containing protein multisystem proteinopathy: Evaluation, diagnosis, and management.American heart journal plus : cardiology research and practice · 2025Review
- Heat shock protein 22: A new direction for cardiovascular disease (Review).Molecular medicine reports · 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
- New Insights into Cardiovascular Diseases Treatment Based on Molecular Targets.International journal of molecular sciences · 2023Review
- Toll-like Receptor 4 Inflammatory Perspective on Doxorubicin-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2023Review
- Heat Shock Protein 22 in Physiological and Pathological Hearts: Small Molecule, Large Potentials.Cells · 2021Review
- Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis.Bioengineered · 2021Article
- Article
- 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
- Insights of heat shock protein 22 in the cardiac protection against ischemic oxidative stress.Redox biology · 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
- Heat Shock Protein 22 Attenuates Doxorubicin-Induced CardiotoxicityFrontiers in pharmacology · 2020Article
- HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation.Redox biology · 2019Article
- VCP represses pathological cardiac hypertrophy.Aging · 2017Article
- The valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.Aging cell · 2017Article
- The valosin-containing protein is a novel mediator of mitochondrial respiration and cell survival in the heart in vivo.Scientific reports · 2017Article
- Cardiac-Restricted Expression of VCP/TER94 RNAi or Disease Alleles PerturbsJournal of cardiovascular development and disease · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsExpression of the heat shock protein 22 (Hsp22) in the heart stimulates cardiac cell survival through activation of the Akt pathway and expression of the inducible nitric oxide (NO) synthase (iNOS), the mediator of ischaemic preconditioning and the most powerful prophylaxis against cardiac cell death. The goal of the present study was to elucidate the downstream effector by which Hsp22 and Akt increase iNOS expression. We tested both in vivo and in vitro the hypothesis that such an effector is the valosin-containing protein (VCP), an Akt substrate, which activates the transcription factor NF-κB, using a transgenic mouse with cardiac-specific over-expression of Hsp22, as well as isolated rat cardiac myocytes. METHODS AND
resultsUsing two-dimensional gel electrophoresis and mass spectrometry combined with immunoprecipitation, we found that Hsp22 and Akt co-localize and interact together with VCP. Adeno-mediated over-expression of VCP in isolated cardiac myocytes activated NF-κB and dose-dependently increased the expression of iNOS, which was abolished upon NF-κB inhibition. Over-expression of a dominant-negative (DN) mutant of VCP did not increase iNOS expression. VCP, but not its DN mutant, protected against chelerythrine-induced apoptosis, which was suppressed by inhibition of either NF-κB or iNOS. VCP-mediated activation of the NF-κB/iNOS pathway was also prevented upon inhibition of Akt.
conclusionWe conclude that the Akt substrate, VCP, mediates the increased expression of iNOS downstream from Hsp22 through an NF-κB-dependent mechanism.
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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.