ArticleNature communications2017
The giant protein titin regulates the length of the striated muscle thick filament.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
66 citing papers in PubMed.
- Four New Muscle Myosin II Binding Properties of Titin: Implications for Myofibrillogenesis.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis.Nature cardiovascular research · 2026Article
- Review
- Titin's P-zone domains A164-167 are essential for thick filament structural arrangement.The Journal of general physiology · 2026Article
- A primer on the methods of skeletal and cardiac muscle mechanics using permeabilized preparations.The Journal of general physiology · 2026Review
- Myosin Filaments of Vertebrate Skeletal and Cardiac Muscle are Highly Similar, but not Identical.bioRxiv : the preprint server for biology · 2026Article
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Comparing cryo-EM structures of the vertebrate cardiac muscle thick filament.Biophysical reviews · 2026Article
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Titin's Intrinsically Disordered PEVK Domain Modulates Actin Polymerization.International journal of molecular sciences · 2025Article
- Titin-dependent biomechanical feedback tailors sarcomeres to specialized muscle functions in insects.Science advances · 2025Article
- Marfan syndrome cardiomyocytes show excess of titin isoform N2BA and extended sarcomeric M-band.The Journal of general physiology · 2025Article
- Visualizing sarcomere and cellular dynamics in skeletal muscle to improve cell therapies.eLife · 2024Article
- Pathomechanisms of Monoallelic variants in TTN causing skeletal muscle disease.Human molecular genetics · 2024Article
- Transient titin-dependent ventricular defects during development lead to adult atrial arrhythmia and impaired contractility.iScience · 2024Article
- Truncated titin is structurally integrated into the human dilated cardiomyopathic sarcomere.The Journal of clinical investigation · 2024Article
- An optimized approach to study nanoscale sarcomere structure utilizing super-resolution microscopy with nanobodies.PloS one · 2024Article
- Titin: roles in cardiac function and diseases.Frontiers in physiology · 2024Review
- Muscle-fiber specific genetic manipulation ofFrontiers in physiology · 2024Article
- Mechanism-based myofilament manipulation to treat diastolic dysfunction in HFpEF.Frontiers in physiology · 2024Review
6 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
8 authors.
Funding
Abstract
The contractile machinery of heart and skeletal muscles has as an essential component the thick filament, comprised of the molecular motor myosin. The thick filament is of a precisely controlled length, defining thereby the force level that muscles generate and how this force varies with muscle length. It has been speculated that the mechanism by which thick filament length is controlled involves the giant protein titin, but no conclusive support for this hypothesis exists. Here we show that in a mouse model in which we deleted two of titin's C-zone super-repeats, thick filament length is reduced in cardiac and skeletal muscles. In addition, functional studies reveal reduced force generation and a dilated cardiomyopathy (DCM) phenotype. Thus, regulation of thick filament length depends on titin and is critical for maintaining muscle health.
Indexed as
Identifiers
What OpenQuestion holds
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.