ReviewJournal of molecular and cellular cardiology2014
Proteotoxicity: an underappreciated pathology in cardiac disease.
Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 66 citations in OpenAlex.
- Mitochondria Take Up and Dispose of Cytosolic Protein Aggregates.Circulation research · 2026Article
- Sex differences in cardiac recovery and ventricular gene expression in a rat model of donation after circulatory death.Biology of sex differences · 2026Article
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer's-like neuropathology.Basic research in cardiology · 2025Article
- Hyperactive mTORC1/4EBP1 signaling dysregulates proteostasis and accelerates cardiac aging.GeroScience · 2025Article
- Paralogue-Specific Roles of SUMO1 and SUMO2/3 in Protein Quality Control and Associated Diseases.Cells · 2023Review
- Genetic control of the dynamic transcriptional response to immune stimuli and glucocorticoids at single cell resolution.bioRxiv : the preprint server for biology · 2022Article
- Article
- Glutathione: A Samsonian life-sustaining small molecule that protects against oxidative stress, ageing and damaging inflammation.Frontiers in nutrition · 2022Review
- Sensing, signaling and surviving mitochondrial stress.Cellular and molecular life sciences : CMLS · 2021Review
- Emerging Role of Mitophagy in the Heart: Therapeutic Potentials to Modulate Mitophagy in Cardiac Diseases.Oxidative medicine and cellular longevity · 2021Review
- Editorial: New Drug Targets for Proteotoxicity in Cardiometabolic Diseases.Frontiers in physiology · 2021Article
- Editorial: Targeting Cardiac Proteotoxicity.Frontiers in physiology · 2021Article
- CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury.Nature communications · 2020Article
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- Ube2v1 Positively Regulates Protein Aggregation by Modulating Ubiquitin Proteasome System Performance Partially Through K63 Ubiquitination.Circulation research · 2020Article
- Mitochondrial Quality Control: Role in Cardiac Models of Lethal Ischemia-Reperfusion Injury.Cells · 2020Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
- Altered C10 domain in cardiac myosin binding protein-C results in hypertrophic cardiomyopathy.Cardiovascular research · 2019Article
- Irreversible oxidative post-translational modifications in heart disease.Expert review of proteomics · 2019Review
- Intermittent Fasting Reverses an Advanced Form of Cardiomyopathy.Journal of the American Heart Association · 2019Article
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 at 2 institutions in 2 countries.
Funding
Abstract
In general, in most organ systems, intracellular protein homeostasis is the sum of many factors, including chromosomal state, protein synthesis, post-translational processing and transport, folding, assembly and disassembly into macromolecular complexes, protein stability and clearance. In the heart, there has been a focus on the gene programs that are activated during pathogenic processes, but the removal of damaged proteins and organelles has been underappreciated as playing an important role in the pathogenesis of heart disease. Proteotoxicity refers to the adverse effects of damaged or misfolded proteins and even organelles on the cell. At the cellular level, the ultimate outcome of uncontrolled or severe proteotoxicity is cell death; hence, the pathogenic impact of proteotoxicity is maximally manifested in organs with no or very poor regenerative capability such as the brain and the heart. Evidence for increased cardiac proteotoxicity is rapidly mounting for a large subset of congenital and acquired human heart disease. Studies carried out in animal models and in cell culture have begun to establish both sufficiency and, in some cases, the necessity of proteotoxicity as a major pathogenic factor in the heart. This dictates rigorous testing for the efficacy of proteotoxic attenuation as a new strategy to treat heart disease. This review article highlights some recent advances in our understanding of how misfolded proteins can injure and are handled in the cell, examining the emerging evidence for targeting proteotoxicity as a new therapeutic strategy for heart disease. This article is part of a Special Issue entitled "Protein Quality Control, the Ubiquitin Proteasome System, and Autophagy."
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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.