ArticleProceedings of the National Academy of Sciences of the United States of America2014
Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 89 citations in OpenAlex.
- Early cardiac proteomic profiling in a long-latency doxorubicin cardiomyopathy model exhibits sexual dimorphism for cardioprotection.Journal of molecular and cellular cardiology plus · 2026Article
- To B-E3 or Not to B-E3: The Roles of MuRF1 and Junctophilin-2 in Junctin Regulation.JACC. Basic to translational science · 2026Article
- JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes.JACC. Basic to translational science · 2026Article
- Elevational variation in heart mass and suppression of hypoxia-induced right ventricle hypertrophy in Andean leaf-eared mice (Phyllotis).The Journal of physiology · 2026Article
- S165F mutation-induced Junctophilin-2 autoinhibition impairs CaCommunications biology · 2025Article
- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Elevational variation in heart mass and suppression of hypoxia-induced right ventricle hypertrophy in Andean leaf-eared mice (bioRxiv : the preprint server for biology · 2025Article
- Virally delivered CMYA5 enhances the assembly of cardiac dyads.Nature biomedical engineering · 2025Article
- Preventing Site-Specific Calpain Proteolysis of Junctophilin-2 Protects Against Stress-Induced Excitation-Contraction Uncoupling and Heart Failure Development.Circulation · 2025Article
- Efficacy of a cysteine protease inhibitor compared with enalapril in murine heart failure models.iScience · 2024Article
- Augmenting workload drives T-tubule assembly in developing cardiomyocytes.The Journal of physiology · 2024Article
- Regulation of cardiomyocyte intracellular trafficking and signal transduction by protein palmitoylation.Biochemical Society transactions · 2024Article
- Structure, Function, and Regulation of the Junctophilin Family.Annual review of physiology · 2024Review
- The Effects of Aging on Sarcoplasmic Reticulum-Related Factors in the Skeletal Muscle of Mice.International journal of molecular sciences · 2024Article
- Ion channel trafficking implications in heart failure.Frontiers in cardiovascular medicine · 2024Review
- Microtubule-Mediated Regulation of βCirculation research · 2023Article
- Article
- DNA Methylation Analysis Identifies Novel Epigenetic Loci in Dilated Murine Heart upon Exposure to Volume Overload.International journal of molecular sciences · 2023Article
- Three-dimensional visualization of the cardiac ryanodine receptor clusters and the molecular-scale fraying of dyads.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Sustained over-expression of calpain-2 induces age-dependent dilated cardiomyopathy in mice through aberrant autophagy.Acta pharmacologica Sinica · 2022Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Heart failure is accompanied by a loss of the orderly disposition of transverse (T)-tubules and a decrease of their associations with the junctional sarcoplasmic reticulum (jSR). Junctophilin-2 (JP2) is a structural protein responsible for jSR/T-tubule docking. Animal models of cardiac stresses demonstrate that down-regulation of JP2 contributes to T-tubule disorganization, loss of excitation-contraction coupling, and heart failure development. Our objective was to determine whether JP2 overexpression attenuates stress-induced T-tubule disorganization and protects against heart failure progression. We therefore generated transgenic mice with cardiac-specific JP2 overexpression (JP2-OE). Baseline cardiac function and Ca(2+) handling properties were similar between JP2-OE and control mice. However, JP2-OE mice displayed a significant increase in the junctional coupling area between T-tubules and the SR and an elevated expression of the Na(+)/Ca(2+) exchanger, although other excitation-contraction coupling protein levels were not significantly changed. Despite similar cardiac function at baseline, overexpression of JP2 provided significantly protective benefits after pressure overload. This was accompanied by a decreased percentage of surviving mice that developed heart failure, as well as preservation of T-tubule network integrity in both the left and right ventricles. Taken together, these data suggest that strategies to maintain JP2 levels can prevent the progression from hypertrophy to heart failure.
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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.