ReviewTrends in molecular medicine2013
Breaking down protein degradation mechanisms in cardiac muscle.
Review in Trends in molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Reduction of Filamin C Results in Altered Proteostasis, Cardiomyopathy, and Arrhythmias.Journal of the American Heart Association · 2024Article
- Sarcomeric network analysis of ex vivo cultivated human atrial appendage tissue using super-resolution microscopy.Scientific reports · 2023Article
- Chaperone-mediated autophagy protects cardiomyocytes against hypoxic-cell death.American journal of physiology. Cell physiology · 2022Article
- Desmosomes: emerging pathways and non-canonical functions in cardiac arrhythmias and disease.Biophysical reviews · 2021Review
- Titin N2A Domain and Its Interactions at the Sarcomere.International journal of molecular sciences · 2021Review
- The Role of HECT-Type E3 Ligase in the Development of Cardiac Disease.International journal of molecular sciences · 2021Review
- Desmosomal COP9 regulates proteome degradation in arrhythmogenic right ventricular dysplasia/cardiomyopathy.The Journal of clinical investigation · 2021Article
- 2-D08 treatment regulates C2C12 myoblast proliferation and differentiation via the Erk1/2 and proteasome signaling pathways.Journal of muscle research and cell motility · 2021Article
- Emerging Strategies Targeting Catabolic Muscle Stress Relief.International journal of molecular sciences · 2020Review
- Gallic Acid Ameliorates Angiotensin II-Induced Atrial Fibrillation by Inhibiting Immunoproteasome- Mediated PTEN Degradation in Mice.Frontiers in cell and developmental biology · 2020Article
- Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Insulin Sensitivity and Glucose Homeostasis Can Be Influenced by Metabolic Acid Load.Nutrients · 2018Review
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Aberrant Protein Turn-Over Associated With Myofibrillar Disorganization in FHL1 Knockout Mice.Frontiers in genetics · 2018Article
- The Calcineurin-FoxO-MuRF1 signaling pathway regulates myofibril integrity in cardiomyocytes.eLife · 2017Article
- Cardiac ubiquitin ligases: Their role in cardiac metabolism, autophagy, cardioprotection and therapeutic potential.Biochimica et biophysica acta · 2016Review
- Modeling and Genome-Editing Brugada Syndrome in a Dish.Journal of the American College of Cardiology · 2016Article
- Desmosomal junctions are necessary for adult sinus node function.Cardiovascular research · 2016Article
- Mechanotransduction in cardiac hypertrophy and failure.Circulation research · 2015Review
- Autophagy and ubiquitination in cardiovascular diseases.DNA and cell biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Regulated protein degradation through the ubiquitin-proteasome and lysosomal/autophagy systems is critical for homeostatic protein turnover in cardiac muscle and for proper cardiac function. The discovery of muscle-specific components in these systems has illuminated how aberrations in their levels are pivotal to the development of cardiac stress and disease. New evidence suggests that equal importance in disease development should be given to ubiquitously expressed degradation components. These are compartmentalized within cardiac muscles and, when mislocalized, can be critical in the development of specific cardiac diseases. Here, we discuss how alterations in the compartmentalization of degradation components affect disease states, the tools available to investigate these mechanisms, as well as recent discoveries that highlight the therapeutic value of targeting these pathways in disease.
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What OpenQuestion holds
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.