ArticleJournal of molecular and cellular cardiology2011
Contribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 72 citations in OpenAlex.
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Titin's P-zone domains A164-167 are essential for thick filament structural arrangement.The Journal of general physiology · 2026Article
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- Rbm20 antisense oligonucleotides alleviate diastolic dysfunction in a mouse model of cardiometabolic heart failure (HFpEF).Cardiovascular research · 2025Article
- Theoretical analysis of power-law stress relaxation and calcium-dependent passive mechanics in cardiac muscle.The Journal of physiology · 2025Article
- Myocardium From Patients With ATTR Amyloidosis Produces Less Force Secondary to Increased Fibrosis.JACC. Basic to translational science · 2025Article
- Mechanism-based myofilament manipulation to treat diastolic dysfunction in HFpEF.Frontiers in physiology · 2024Review
- The microtubule cytoskeleton in cardiac mechanics and heart failure.Nature reviews. Cardiology · 2022Review
- Shortening the thick filament by partial deletion of titin's C-zone alters cardiac function by reducing the operating sarcomere length range.Journal of molecular and cellular cardiology · 2022Article
- Functional and structural differences between skinned and intact muscle preparations.The Journal of general physiology · 2022Review
- RBM20, a Therapeutic Target to Alleviate Myocardial StiffnessFrontiers in cardiovascular medicine · 2022Review
- Increased Expression of N2BA Titin Corresponds to More Compliant Myofibrils in Athlete's Heart.International journal of molecular sciences · 2021Article
- Comparison of the histology and stiffness of ventricles in Anura of different habitats.Journal of biological physics · 2021Article
- Reduced preload increases Mechanical Control (strain-rate dependence) of Relaxation by modifying myosin kinetics.Archives of biochemistry and biophysics · 2021Article
- Paired Pressure-Volume Loop Analysis and Biaxial Mechanical Testing Characterize Differences in Left Ventricular Tissue Stiffness of Volume Overload and Angiotensin-Induced Pressure Overload Hearts.Journal of biomechanical engineering · 2021Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- High efficiency preparation of skinned mouse cardiac muscle strips from cryosections for contractility studies.Experimental physiology · 2020Article
- Phosphodiesterase 9a Inhibition in Mouse Models of Diastolic Dysfunction.Circulation. Heart failure · 2020Article
- Effects of Adiponectin on Diastolic Function in Mice Underwent Transverse Aorta Constriction.Journal of cardiovascular translational research · 2020Article
- Stretching single titin molecules from failing human hearts reveals titin's role in blunting cardiac kinetic reserve.Cardiovascular research · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It remains to be established to what degree titin and the extracellular matrix (ECM) contribute to passive pressure in the left ventricle (LV). Thus, we aimed to elucidate the contribution of major molecular determinants of passive pressure in the normal mouse LV. Furthermore, we determined the working sarcomere length (SL) range of the LV to bridge our findings to earlier work in skinned muscle fibers. We utilized Frank-Starling type protocols to obtain diastolic pressure-volume relationships (PVR) in Langendorff perfused isolated LVs. To quantify the molecular contribution of titin and ECM, we innovated on methods of fiber mechanics to chemically permeabilize intact LVs and measure a fully passive PVR. To differentially dissect the contributions of the ECM and titin, we utilized myofilament extraction techniques in permeabilized LVs, measuring passive PVRs at each stage in the protocol. Myofilament extraction suggests that titin contributes ~80% of passive pressures in the heart. Langendorff perfusion was also used to chemically fix passive and BaCl(2) activated hearts at specific volumes to determine that the maximal working SL range of the midwall LV fibers is approximately 1.8-2.2 μm. A model of the passive SL-volume relationship was then used to estimate the pressure-SL relationships, indicating that the ECM contribution does not exceed titin's contribution until large volumes with SLs >~2.2 μm. In conclusion, within physiological volumes, titin is the dominant contributor to LV passive pressure, and ECM-based pressures dominate at larger volumes.
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