ReviewCirculation research2015
Proteotoxicity and cardiac dysfunction.
Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
70 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- MicroRNAs in Takotsubo Syndrome: A Systematic Review of Regulatory Networks in Stress-Induced Cardiomyopathy.International journal of molecular sciences · 2025Pooled it
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- Early pre-symptomatic and sex-specific cardiac remodeling precedes heart failure in zebrafish with a human actin variant.Disease models & mechanisms · 2026Article
- Nrf1 coordinates proteasome activity and autophagy to maintain cardiac proteostasis.Communications biology · 2026Article
- Article
- Redox Imbalance and Genetic Mutations in Heart Failure: Synergistic Mechanisms and Therapeutic Strategies.Genes · 2026Review
- Genomic structural equation modeling reveals shared genetic structure of cardiac function and structure-function association studies of CLCNKA mutations.Scientific reports · 2026Article
- Dose- and genotype-dependent cardiac arrhythmia and sudden death in rats following microdystrophin gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- First Glance at Myeloid Leukaemia Factor 2 in Cardiomyocytes.Journal of cardiovascular development and disease · 2025Article
- A microbial community that alters mitochondrial morphology and age-related motor function iniScience · 2025Article
- Peptidyl-tRNA hydrolase 2 is a negative regulator of peripartum cardiomyopathy with heart failure in female mice.Nature communications · 2025Article
- An mTOR-Tfeb-Fabp7a Axis Ameliorates bag3 Cardiomyopathy via Decelerating Cardiac Aging.Aging cell · 2025Article
- Current Understanding of Protein Aggregation in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer's-like neuropathology.Basic research in cardiology · 2025Article
- The deubiquitinase USP5 prevents accumulation of protein aggregates in cardiomyocytes.Science advances · 2025Article
- Caloric restriction and its mimetics in heart failure with preserved ejection fraction: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
- Cardiac fibroblast BAG3 regulates TGFBR2 signaling and fibrosis in dilated cardiomyopathy.The Journal of clinical investigation · 2025Article
- Zebrafish as a model for crystallin-associated congenital cataracts in humans.Frontiers in cell and developmental biology · 2025Review
- Exercise training decreases the load and changes the content of circulating SDS-resistant protein aggregates in patients with heart failure with reduced ejection fraction.Molecular and cellular biochemistry · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Baseline physiological function of the mammalian heart is under the constant threat of environmental or intrinsic pathological insults. Cardiomyocyte proteins are thus subject to unremitting pressure to function optimally, and this depends on them assuming and maintaining proper conformation. This review explores the multiple defenses a cell may use for its proteins to assume and maintain correct protein folding and conformation. There are multiple quality control mechanisms to ensure that nascent polypeptides are properly folded and mature proteins maintain their functional conformation. When proteins do misfold, either in the face of normal or pathological stimuli or because of intrinsic mutations or post-translational modifications, they must either be refolded correctly or recycled. In the absence of these corrective processes, they may become toxic to the cell. Herein, we explore some of the underlying mechanisms that lead to proteotoxicity. The continued presence and chronic accumulation of misfolded or unfolded proteins can be disastrous in cardiomyocytes because these misfolded proteins can lead to aggregation or the formation of soluble peptides that are proteotoxic. This in turn leads to compromised protein quality control and precipitating a downward spiral of the cell's ability to maintain protein homeostasis. Some underlying mechanisms are discussed and the therapeutic potential of interfering with proteotoxicity in the heart is explored.
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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.