ArticleProceedings of the National Academy of Sciences of the United States of America2003
Damped elastic recoil of the titin spring in myofibrils of human myocardium.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 124 citations in OpenAlex.
- Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales.Annual review of biomedical engineering · 2026Review
- The genome of the relict earless monitor lizard, Lanthanotus borneensis, and the Toxicofera hypothesis.BMC biology · 2026Article
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Electrically conductive biopolymer-based hydrogels and fibrous materials fabricated using 3D printing and electrospinning for cardiac tissue engineering.Bioactive materials · 2025Review
- Interpreting Diastolic Dynamics and Evaluation through Echocardiography.Life (Basel, Switzerland) · 2024Review
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- RBM20Journal of molecular and cellular cardiology · 2022Article
- Accelerated Mechanochemistry in Helical Polymers.Angewandte Chemie (International ed. in English) · 2022Article
- Lipotoxicity: a driver of heart failure with preserved ejection fraction?Clinical science (London, England : 1979) · 2021Review
- New insights into hallux valgus by whole exome sequencing study.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Small but Smart: On the Diverse Role of Small Proteins in the Regulation of Cyanobacterial Metabolism.Life (Basel, Switzerland) · 2020Review
- N2A Titin: Signaling Hub and Mechanical Switch in Skeletal Muscle.International journal of molecular sciences · 2020Review
- Rapid Peptides Generator: fast and efficientNAR genomics and bioinformatics · 2020Article
- Efficient inference of homologs in large eukaryotic pan-proteomes.BMC bioinformatics · 2018Article
- Force properties of skinned cardiac muscle following increasing volumes of aerobic exercise in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Applying Expression Profile Similarity for Discovery of Patient-Specific Functional Mutations.High-throughput · 2018Article
- The Work of Titin Protein Folding as a Major Driver in Muscle Contraction.Annual review of physiology · 2018Review
- Article
- A map of the phosphoproteomic alterations that occur after a bout of maximal-intensity contractions.The Journal of physiology · 2017Article
- Hydraulic forces contribute to left ventricular diastolic filling.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The giant protein titin functions as a molecular spring in muscle and is responsible for most of the passive tension of myocardium. Because the titin spring is extended during diastolic stretch, it will recoil elastically during systole and potentially may influence the overall shortening behavior of cardiac muscle. Here, titin elastic recoil was quantified in single human heart myofibrils by using a high-speed charge-coupled device-line camera and a nanonewtonrange force sensor. Application of a slack-test protocol revealed that the passive shortening velocity (Vp) of nonactivated cardiomyofibrils depends on: (i) initial sarcomere length, (ii) release-step amplitude, and (iii) temperature. Selective digestion of titin, with low doses of trypsin, decelerated myofibrillar passive recoil and eventually stopped it. Selective extraction of actin filaments with a Ca2+-independent gelsolin fragment greatly reduced the dependency of Vp on release-step size and temperature. These results are explained by the presence of viscous forces opposing myofibrillar passive recoil that are caused mainly by weak actin-titin interactions. Thus, Vp is determined by two distinct factors: titin elastic recoil and internal viscous drag forces. The recoil could be modeled as that of a damped entropic spring consisting of independent worm-like chains. The functional importance of myofibrillar elastic recoil was addressed by comparing instantaneous Vp to unloaded shortening velocity, which was measured in demembranated, fully Ca2+-activated, human cardiac fibers. Titin-driven passive recoil was much faster than active unloaded shortening velocity in early phases of isotonic contraction. Damped myofibrillar elastic recoil could help accelerate active contraction speed of human myocardium during early systolic shortening.
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.