ArticleCirculation research2018
Desmin Phosphorylation Triggers Preamyloid Oligomers Formation and Myocyte Dysfunction in Acquired Heart Failure.
Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.The Journal of physiology · 2026Pooled it
- Mitophagy Facilitates Cytosolic Proteostasis to Preserve Cardiac Function.Circulation research · 2026Article
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- Failure of efficient cardiac proteostatic adaptations to chronic cAMP-stress is associated with accelerated heart aging.GeroScience · 2026Article
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Chaperone proteins protect against desmin fragment amyloid aggregation.Biophysical journal · 2026Article
- Regulation of mechanical intercellular junctions and components of the mitochondrial electron transport chain and the TCA cycle in the hypertrophic heart by pyridostigmine or trandolapril.Frontiers in molecular biosciences · 2026Article
- BubR1 Insufficiency Drives Transcriptomic Alterations and Pathology Associated With Cardiac Aging and Heart Failure.Aging cell · 2025Article
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Phosphorylation of CRYAB induces a condensatopathy to worsen post-myocardial infarction left ventricular remodeling.The Journal of clinical investigation · 2025Article
- Thioflavin T in-gel staining forFrontiers in molecular biosciences · 2025Article
- Acute resistance exercise and training reduce desmin phosphorylation at serine 31 in human skeletal muscle, making the protein less prone to cleavage.Scientific reports · 2024Article
- Diastolic dysfunction in Alzheimer's disease model mice is associated with Aβ-amyloid aggregate formation and mitochondrial dysfunction.Scientific reports · 2024Article
- Review
- Article
- Considering impact of age and sex on cardiac cytoskeletal components.American journal of physiology. Heart and circulatory physiology · 2024Review
- Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation.Stem cell research & therapy · 2024Article
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue.Antioxidants (Basel, Switzerland) · 2023Article
- Human Neuromuscular Junction on a Chip: Impact of Amniotic Fluid Stem Cell Extracellular Vesicles on Muscle Atrophy and NMJ Integrity.International journal of molecular sciences · 2023Article
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
rationaleDisrupted proteostasis is one major pathological trait that heart failure (HF) shares with other organ proteinopathies, such as Alzheimer and Parkinson diseases. Yet, differently from the latter, whether and how cardiac preamyloid oligomers (PAOs) develop in acquired forms of HF is unclear.
objectiveWe previously reported a rise in monophosphorylated, aggregate-prone desmin in canine and human HF. We now tested whether monophosphorylated desmin acts as the seed nucleating PAOs formation and determined whether positron emission tomography is able to detect myocardial PAOs in nongenetic HF. METHODS AND
resultsHere, we first show that toxic cardiac PAOs accumulate in the myocardium of mice subjected to transverse aortic constriction and that PAOs comigrate with the cytoskeletal protein desmin in this well-established model of acquired HF. We confirm this evidence in cardiac extracts from human ischemic and nonischemic HF. We also demonstrate that Ser31 phosphorylated desmin aggregates extensively in cultured cardiomyocytes. Lastly, we were able to detect the in vivo accumulation of cardiac PAOs using positron emission tomography for the first time in acquired HF.
conclusionsSer31 phosphorylated desmin is a likely candidate seed for the nucleation process leading to cardiac PAOs deposition. Desmin post-translational processing and misfolding constitute a new, attractive avenue for the diagnosis and treatment of the cardiac accumulation of toxic PAOs that can now be measured by positron emission tomography in acquired HF.
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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.