ArticleThe Journal of biological chemistry2011
Muscle creatine kinase deficiency triggers both actin depolymerization and desmin disorganization by advanced glycation end products in dilated cardiomyopathy.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications.International journal of molecular sciences · 2025Review
- Interrelation between α-Cardiac Actin Treadmilling and Myocardin-Related Transcription Factor-A Nuclear Shuttling in Cardiomyocytes.International journal of molecular sciences · 2022Article
- What does desmin do: A bibliometric assessment of the functions of the muscle intermediate filament.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Rabphilin silencing causes dilated cardiomyopathy in a Drosophila model of nephrocyte damage.Scientific reports · 2021Article
- Desmin aggrephagy in rat and human ischemic heart failure through PKCζ and GSK3β as upstream signaling pathways.Cell death discovery · 2021Article
- NMRK2 Gene Is Upregulated in Dilated Cardiomyopathy and Required for Cardiac Function and NAD Levels during Aging.International journal of molecular sciences · 2021Article
- Article
- Creatine kinase/α-crystallin interaction functions in cataract development.Biochemistry and biophysics reports · 2020Article
- NADFrontiers in physiology · 2020Review
- Intermediate filaments in cardiomyopathy.Biophysical reviews · 2018Review
- Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.Circulation · 2018Article
- Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.American journal of physiology. Heart and circulatory physiology · 2017Article
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- A comprehensive characterisation of the metabolic profile of varicose veins; implications in elaborating plausible cellular pathways for disease pathogenesis.Scientific reports · 2017Article
- Amotl1 mediates sequestration of the Hippo effector Yap1 downstream of Fat4 to restrict heart growth.Nature communications · 2017Article
- Voluntary Exercise Improves Cardiac Function and Prevents Cardiac Remodeling in a Mouse Model of Dilated Cardiomyopathy.Frontiers in physiology · 2017Article
- Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and mitochondrial functions.Glycoconjugate journal · 2016Review
- Increased level of phosphorylated desmin and its degradation products in heart failure.Biochemistry and biophysics reports · 2016Article
- Serum Response Factor in Muscle Tissues: From Development to Ageing.European journal of translational myology · 2016Article
- Creatine kinase B is necessary to limit myoblast fusion during myogenesis.American journal of physiology. Cell physiology · 2015Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in the balance of cytoskeleton as well as energetic proteins are involved in the cardiac remodeling occurring in dilated cardiomyopathy (DCM). We used two-dimensional DIGE proteomics as a discovery approach to identify key molecular changes taking place in a temporally controlled model of DCM triggered by cardiomyocyte-specific serum response factor (SRF) knock-out in mice. We identified muscle creatine kinase (MCK) as the primary down-regulated protein followed by α-actin and α-tropomyosin down-regulation leading to a decrease of polymerized F-actin. The early response to these defects was an increase in the amount of desmin intermediate filaments and phosphorylation of the αB-crystallin chaperone. We found that αB-crystallin and desmin progressively lose their striated pattern and accumulate at the intercalated disk and the sarcolemma, respectively. We further show that desmin is a preferential target of advanced glycation end products (AGE) in mouse and human DCM. Inhibition of CK in cultured cardiomyocytes is sufficient to recapitulate both the actin depolymerization defect and the modification of desmin by AGE. Treatment with either cytochalasin D or glyoxal, a cellular AGE, indicated that both actin depolymerization and AGE contribute to desmin disorganization. Heat shock-induced phosphorylation of αB-crystallin provides a transient protection of desmin against glyoxal in a p38 MAPK-dependent manner. Our results show that the strong down-regulation of MCK activity contributes to F-actin instability and induces post-translational modification of αB-crystallin and desmin. Our results suggest that AGE may play an important role in DCM because they alter the organization of desmin filaments that normally support stress response and mitochondrial functions in cardiomyocytes.
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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.