Piezometric architecture and the geometry of plasticity: a proposed electromechanical model of the Fibrosis–Plasticity axis

Background Models of fibrosis are largely molecular and cell-centred. How whole-organism load geometry constrains long-term tissue fate is comparatively underspecified. The Fibrosis–Plasticity Axis (FPA), a conceptual continuum from reversible remodelling capacity to structural fixation, is proposed here as an organising frame; the physical steps linking load geometry to position on that continuum have not been articulated as a testable chain. Objective To formulate, and render falsifiable, the hypothesis that deformation-generated electrical phenomena in collagen-rich matrix act as a load-geometry-dependent modulator of remodelling, and to define the constructs required to test it. Approach We synthesise evidence from tissue electromechanics, mechanotransduction and connective-tissue physiology, and grade each proposed causal link by evidence level. Proposed framework We introduce, as constructs original to this work: the Geometric Origin of the Body (GOB), the equilibrium configuration around which load-bearing architecture is organised; the Geometric Optimal Pressure Load (GOPeL), the hypothesised load distribution permitting maximal reversibility; and the Geometric Origin Displacement Index (GODI), a proposed—not operationalised, not validated—index of deviation from GOB. The electromechanical proposal is stated as three nested hypotheses. H1, the broad electromechanical hypothesis, holds that deformation of collagen-rich matrix generates local electrical phenomena—electrokinetic, piezoelectric and potentially flexoelectric—which may modulate the behaviour of matrix-producing cells. H2, nested within H1, holds that a solid-state component contributes at physiological hydration and, because it does not require fluid flow for its generation, would be expected to persist when electrokinetic contributions are reduced. H3, nested within H2, holds that this solid-state component is specifically piezoelectric rather than flexoelectric. Each may fail without the one above it failing. We further propose that chronic load asymmetry is distributed through mechanically continuous tissue and generates locally biased electrical signalling at many sites, rather than an electrical field propagating through the organism. Key discriminating criterion If cellular remodelling phenotype is unchanged when electromechanically active and electrically inert matrices are compared under matched mechanical exposure, across the substrate, cell type and loading regimes tested, the electrical contribution proposed here would not be supported within that experimental domain.