ReviewNature reviews. Cardiology2017
Proteostasis in cardiac health and disease.
Review in Nature reviews. Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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
109 citing papers in PubMed, 178 citations in OpenAlex.
- Acetyl-CoA synthetase 2 maintains cytosolic acetyl-CoA homeostasis to preserve mitochondrial integrity and attenuate cardiac dysfunction under chronic β-adrenergic stress.Journal of molecular and cellular cardiology plus · 2026Article
- Stimulating proteasomal degradation in human proteinopathies.The FEBS journal · 2026Review
- Review
- The role of sleep disorders in orchestrating proteomic dysfunction and multi-morbidity.Molecular psychiatry · 2026Review
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Nrf1 coordinates proteasome activity and autophagy to maintain cardiac proteostasis.Communications biology · 2026Article
- Genomic Structural Equation Modeling Reveals Cardiovascular-Kidney-Metabolic Syndrome Genetic Architecture.Journal of diabetes · 2026Article
- Mechanisms of Atrial Fibrillation in Heart Failure: Uncovering Therapeutic Targets in the Atrial Substrate.Current heart failure reports · 2026Review
- Endoplasmic Reticulum Stress Induced by Turbulence of Mitochondrial Fusion and Fission Was Involved in Isoproterenol-Induced H9c2 Cell Injury.International journal of molecular sciences · 2026Article
- Geranylgeranylacetone as Prevention for Postoperative Atrial Fibrillation (GENIALITY).Cardiovascular drugs and therapy · 2025Article
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- FICD (FIC Domain Protein Adenylyl Transferase) Deficiency Protects Mice From Hypertrophy-Induced Heart Failure and Promotes BiP (Binding Immunoglobulin Protein) -Mediated Activation of the Unfolded Protein Response and Endoplasmic Reticulum-Selective Autophagy in Cardiomyocytes.Journal of the American Heart Association · 2025Article
- TRIM24 regulates chromatin remodeling and calcium dynamics in cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- The Interplay Between Pulmonary Hypertension and Atrial Fibrillation: A Comprehensive Overview.Cells · 2025Review
- Proteostasis and Its Role in Disease Development.Cell biochemistry and biophysics · 2025Review
- cIAP2-mediated IGF2BP2 ubiquitination and degradation regulate cardiomyocyte apoptosis via stabilizing mCell biology and toxicology · 2025Article
- Proteostatic Imbalance Drives the Pathogenesis and Age-Related Exacerbation of Heart Failure With Preserved Ejection Fraction.JACC. Basic to translational science · 2025Article
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Therapeutic potential and mechanistic insights of astragaloside IV in the treatment of arrhythmia: a comprehensive review.Frontiers in pharmacology · 2025Review
49 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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence and prevalence of cardiac diseases, which are the main cause of death worldwide, are likely to increase because of population ageing. Prevailing theories about the mechanisms of ageing feature the gradual derailment of cellular protein homeostasis (proteostasis) and loss of protein quality control as central factors. In the heart, loss of protein patency, owing to flaws in genetically-determined design or because of environmentally-induced 'wear and tear', can overwhelm protein quality control, thereby triggering derailment of proteostasis and contributing to cardiac ageing. Failure of protein quality control involves impairment of chaperones, ubiquitin-proteosomal systems, autophagy, and loss of sarcomeric and cytoskeletal proteins, all of which relate to induction of cardiomyocyte senescence. Targeting protein quality control to maintain cardiac proteostasis offers a novel therapeutic strategy to promote cardiac health and combat cardiac disease. Currently marketed drugs are available to explore this concept in the clinical setting.
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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.