ReviewJournal of molecular and cellular cardiology2020
Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.
Review in Journal of molecular and cellular cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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
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Who cites it
54 citing papers in PubMed.
- Contractility Drives Cardiomyocyte Maturation and the Response to Nanopatterns.Circulation research · 2026Article
- The formin Fhod3 is required for sarcomere reassembly after mitosis in postnatal cardiomyocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Cell-cycle regulation of sarcomere integrity-Role for Actn2 phosphorylation.Physiological reports · 2026Article
- Multi-omics Insight into Cardiac Myofibril Remodeling in Post-Prandial Burmese Pythons.bioRxiv : the preprint server for biology · 2026Article
- FHOD3 deficiency disrupts sarcomere organization and activates caMKII signaling in human stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Pharmacological Inhibition of β Myosin II Disrupts Sarcomere Assembly in Human iPSC-Derived Cardiac Myocytes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Dynamic proteome profiling of differentiating human embryonic stem cells towards cardiomyocytes.Scientific reports · 2025Article
- Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025Review
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Uncovering cell type-specific phenotypes using a novel human in vitro model of transthyretin amyloid cardiomyopathy.Stem cell research & therapy · 2025Article
- Comprehensive ubiquitome analysis reveals persistent mitochondrial remodeling disruptions from doxorubicin-induced cardiotoxicity in aged CD-1 male mice.Archives of toxicology · 2025Article
- Major Oxidative and Antioxidant Mechanisms During Heat Stress-Induced Oxidative Stress in Chickens.Antioxidants (Basel, Switzerland) · 2025Review
- α Protein Kinase 3 Is Essential for Neonatal and Adult Cardiac Function.Journal of the American Heart Association · 2025Article
- The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025Review
- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- YAP Overcomes Mechanical Barriers to Induce Mitotic Rounding and Adult Cardiomyocyte Division.Circulation · 2025Article
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 2024Review
- The importance of myosin ubiquitination status for cardiac remodeling: USP20 has entered the chat.American journal of physiology. Heart and circulatory physiology · 2024Article
- Molecular regulation of reversible cardiac remodeling: lessons from species with extreme physiological adaptations.The Journal of experimental biology · 2024Review
- Exercise Alleviates Cardiovascular Diseases by Improving Mitochondrial Homeostasis.Journal of the American Heart Association · 2024Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The sarcomere is the basic contractile unit of striated muscle and is a highly ordered protein complex with the actin and myosin filaments at its core. Assembling the sarcomere constituents into this organized structure in development, and with muscle growth as new sarcomeres are built, is a complex process coordinated by numerous factors. Once assembled, the sarcomere requires constant maintenance as its continuous contraction is accompanied by elevated mechanical, thermal, and oxidative stress, which predispose proteins to misfolding and toxic aggregation. To prevent protein misfolding and maintain sarcomere integrity, the sarcomere is monitored by an assortment of protein quality control (PQC) mechanisms. The need for effective PQC is heightened in cardiomyocytes which are terminally differentiated and must survive for many years while preserving optimal mechanical output. To prevent toxic protein aggregation, molecular chaperones stabilize denatured sarcomere proteins and promote their refolding. However, when old and misfolded proteins cannot be salvaged by chaperones, they must be recycled via degradation pathways: the calpain and ubiquitin-proteasome systems, which operate under basal conditions, and the stress-responsive autophagy-lysosome pathway. Mutations to and deficiency of the molecular chaperones and associated factors charged with sarcomere maintenance commonly lead to sarcomere structural disarray and the progression of heart disease, highlighting the necessity of effective sarcomere PQC for maintaining cardiac function. This review focuses on the dynamic regulation of assembly and turnover at the sarcomere with an emphasis on the chaperones involved in these processes and describes the alterations to chaperones - through mutations and deficient expression - implicated in disease progression to heart failure.
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