ReviewProteomics. Clinical applications2014
Protein post-translational modifications and misfolding: new concepts in heart failure.
Review in Proteomics. Clinical applications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- How soluble misfolded proteins bypass chaperones at the molecular level.Nature communications · 2023Pooled it
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- Lipidation as a post-translational code for protein liquid-liquid phase separation.Journal of lipid research · 2026Review
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- The Identification by Shotgun Proteomics with High-Resolution Tandem Mass-Spectrometry of Histone Isoforms' Hypermethylation Phenotype as a Hallmark Characteristic of Human-IDH-Mutant High-Grade Gliomas: Epigenetic Applications for Genotoxicity-Based Biomarkers and Cancer Therapy Targets.Journal of proteome research · 2025Article
- Particulate matter and co-occurring genetic risk induce oxidative stress and cardiac and brain Alzheimer's pathology.Communications biology · 2025Article
- Diagnostic and Therapeutic Implications of the SUMOylation Pathway in Acute Myeloid Leukemia.Cancers · 2025Review
- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- Thioflavin T in-gel staining forFrontiers in molecular biosciences · 2025Article
- Remodeling of Cardiomyocytes: Study of Morphological Cellular Changes Preceding Symptomatic Ischemic Heart Failure.International journal of molecular sciences · 2023Article
- Pressure overload induces ISG15 to facilitate adverse ventricular remodeling and promote heart failure.The Journal of clinical investigation · 2023Article
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
- Posttranslational modifications in proteins: resources, tools and prediction methods.Database : the journal of biological databases and curation · 2021Article
- Article
- Heart and Brain: Complex Relationships for Left Ventricular Dysfunction.Current cardiology reports · 2020Review
- Review
- Come Together: Protein Assemblies, Aggregates and the Sarcostat at the Heart of Cardiac Myocyte Homeostasis.Frontiers in physiology · 2020Review
- Therapeutic Fc fusion protein misfolding: A three-phasic cultivation experimental design.PloS one · 2019Article
- Intermediate filaments in cardiomyopathy.Biophysical reviews · 2018Review
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
A new concept in the field of heart-failure (HF) research points to a role of misfolded proteins, forming preamyloid oligomers (PAOs), in cardiac toxicity. This is largely based on few studies reporting the presence of PAOs, similar to those observed in neurodegenerative diseases, in experimental and human HF. As the majority of proteinopathies are sporadic in nature, protein post-translational modifications (PTMs) likely play a major role in this growing class of diseases. In fact, PTMs are known regulators of protein folding and of the formation of amyloid species in well-established proteinopathies. Proteomics has been instrumental in identifying both chemical and enzymatic PTMs, with a potential impact on protein mis-/folding. Here we provide the basics on how proteins fold along with a few examples of PTMs known to modulate protein misfolding and aggregation, with particular focus on the heart. Due to its innovative content and the growing awareness of the toxicity of misfolded proteins, an "Alzheimer's theory of HF" is timely. Moreover, the continuous innovations in proteomic technologies will help pinpoint PTMs that could contribute to the process. This nuptial between biology and technology could greatly assist in identifying biomarkers with increased specificity as well as more effective therapies.
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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.