Molecular PhysiologyCardiac thin-filament laboratory
Molecule → sarcomere → ventricle
Watch calcium turn a protein switch into cardiac force.
Compare paired experimental thin-filament structures, manipulate calcium handling, and follow the signal from troponin C occupancy to relative active force.
Experimental structure6KN7 · Calcium-free
Cryo-EM · 6.6 Å
experimentalStructure set
Endpoint state
6KN7Calcium-free thin filament · 6.6 Å
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helixstrandloop
The trace above is an alpha-carbon backbone: helices and strands are coloured rather than drawn as ribbons and arrows, and there is no surface. That is the honest limit of what this viewer draws, not a claim about the structure.
interpolatedTroponin core, calcium-free to calcium-bound
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6KN7 · calcium-freedeposited structure6KN8 · calcium-bound
Atomistic molecular dynamics
Run Newtonian motion on a cardiac calcium sensor.
This workflow prepares an explicit-solvent protein system and executes energy minimization, NPT equilibration, and production dynamics on your RTX 3080.
02 · Production duration
03 · Starting conformer
Estimated scope25 ps productionShort trajectories sample local fluctuations, not equilibrium conformational populations. Running several conformers is what makes a comparison meaningful.
What makes this real
OpenMM integrates an all-atom force field through time on the GPU. Coordinates, energies, temperature, and structural observables come from that trajectory rather than from a hand-drawn animation.
What it cannot establishA 10 to 100 ps trajectory is far too short for binding free energy, mutation pathogenicity, calcium affinity, macroscopic force, or clinical response. Those require replicated, validated protocols and substantially longer sampling.
One cardiac cycle
Calcium rises first. Force follows nonlinearly.
The Hill relationship converts a transient calcium signal into cooperative thin-filament activation. This is a reduced teaching model, not a patient-specific prediction.
Cytosolic Ca²⁺Relative active force
Live multiscale bridge
One molecular change, propagated to the circulation.
Peak thin-filament force sets end-systolic elastance. Preload and arterial load then determine the pressure-volume loop, stroke volume, pressure, and flow.
Ventricular mechanicsPressure-volume loop
currentreference
EDV115 mLESV45 mLSV70 mLEF61%
Normalized thin-filament force is mapped to end-systolic elastance.
Ventricular contractility competes with effective arterial elastance.
Beat volume and vascular resistance determine macroscopic flow and pressure.
This deterministic reduced-order model is designed to teach causal direction and ventricular-arterial coupling. It does not represent regional mechanics, reflex compensation, myocardial energetics, valve disease, or an individual patient.
Mechanistic bridge
Five linked scales of contraction.
Ca²⁺ transient
L-type entry triggers sarcoplasmic-reticulum calcium release.
Troponin C
Regulatory calcium binding stabilizes the activated troponin state.
Tropomyosin
The cable moves across actin and reduces steric inhibition.
Cross-bridges
Myosin gains access to actin and generates sarcomere tension.
Ventricular force
Synchronized myocytes raise chamber elastance and pressure.
Evidence and provenance
Know which parts are observed and which are modeled.
Paired cryo-EM structures of the human cardiac thin filament in calcium-free and calcium-bound conditions.
Re-modeled tropomyosin positions based on the corresponding experimental maps.
Hill activation, end-systolic elastance, and ventricular-arterial coupling propagate molecular force to pressure and flow.
The atomistic console prepares explicit-solvent systems, minimizes them, equilibrates at constant pressure, and records a production trajectory.
Structural endpoints are not a continuous measured movie. Switching between them illustrates state-dependent architecture; the animated physiology trace is an explicitly labeled reduced model.