ArticleJournal of molecular and cellular cardiology2017
Cardiac proteasome functional insufficiency plays a pathogenic role in diabetic cardiomyopathy.
Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- PKA-Mediated Proteasome Activation Protects Against Cardiac Remodeling and Heart Failure During Systolic Overload.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Diabetic cardiomyopathy as a disorder of proteostatic maladaptation: context-dependent ubiquitin-specific protease networks.Frontiers in cell and developmental biology · 2026Review
- Not Just PA28γ: What We Know About the Role of PA28αβ in Carcinogenesis.Biomolecules · 2025Review
- Promoting proteostasis by cAMP/PKA and cGMP/PKG.Trends in molecular medicine · 2025Review
- Interplay between Senescence and Macrophages in Diabetic Cardiomyopathy: A Review of the Potential Role of GDF-15 and Klotho.Biomedicines · 2024Review
- Understanding Diabetic Cardiomyopathy: Insulin Resistance and Beyond.Heart international · 2024Review
- Article
- Heart Failure And Type 2 Diabetes Mellitus: Neurohumoral, Histological And Molecular Interconnections.Current cardiology reviews · 2023Review
- The double-hit protocol induces HFpEF and impairs myocardial ubiquitin-proteasome system performance in FVB/N mice.Frontiers in physiology · 2023Article
- Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development.Frontiers in physiology · 2022Review
- Osteocrin, a novel myokine, prevents diabetic cardiomyopathy via restoring proteasomal activity.Cell death & disease · 2021Article
- The Diabetic Cardiomyopathy: The Contributing Pathophysiological Mechanisms.Frontiers in medicine · 2021Review
- The Calcineurin-TFEB-p62 Pathway Mediates the Activation of Cardiac Macroautophagy by Proteasomal Malfunction.Circulation research · 2020Article
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- The phospholamban p.(Arg14del) pathogenic variant leads to cardiomyopathy with heart failure and is unreponsive to standard heart failure therapy.Scientific reports · 2020Article
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- PDE1 inhibition facilitates proteasomal degradation of misfolded proteins and protects against cardiac proteinopathy.Science advances · 2019Article
- Proteasome biology and therapeutics in cardiac diseases.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Diabetic cardiomyopathy: molecular mechanisms, detrimental effects of conventional treatment, and beneficial effects of natural therapy.Heart failure reviews · 2019Review
- Highly Dynamic Changes in the Activity and Regulation of Macroautophagy in Hearts Subjected to Increased Proteotoxic Stress.Frontiers in physiology · 2019Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundDiabetic cardiomyopathy is a major risk factor in diabetic patients but its pathogenesis remains poorly understood. The ubiquitin-proteasome system (UPS) facilitates protein quality control by degrading unnecessary and damaged proteins in eukaryotic cells, and dysfunction of UPS is implicated in various cardiac diseases. However, the overall functional status of the UPS and its pathophysiological role in diabetic cardiomyopathy have not been determined. METHODS AND
resultsType I diabetes was induced in wild-type and transgenic mice expressing a UPS functional reporter (GFPdgn) by injections of streptozotocin (STZ). STZ-induced diabetes progressively impaired cardiac UPS function as evidenced by the accumulation of GFPdgn proteins beginning two weeks after diabetes induction, and by a buildup of total and lysine (K) 48-linked polyubiquitinated proteins in the heart. To examine the functional role of the UPS in diabetic cardiomyopathy, cardiac overexpression of PA28α (PA28αOE) was used to enhance proteasome function in diabetic mouse hearts. PA28αOE diabetic mice displayed exhibited restoration of cardiac UPS function, as demonstrated by the diminished accumulation of GFPdgn and polyubiquitinated proteins. Moreover, PA28αOE diabetic mice exhibited reduced myocardial collagen deposition, decreased cardiomyocyte apoptosis, and improved cardiac systolic and diastolic function.
conclusionImpairment of cardiac UPS function is an early event in STZ-induced diabetes. Overexpression of PA28α attenuates diabetes-induced proteotoxic stress and cardiomyopathy, suggesting a potential therapeutic role for enhancement of cardiac proteasome function in this disorder.
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