Key result
Solute diffusion in murine cardiac myocytes is highly restricted by myofilaments and mitochondrial networks, with diffusion being 2.5-fold more restricted in myocytes lacking the mitochondrial porin Vdac1.
Why the study?
It was unknown whether solute diffusion restrictions in cardiac cytoplasm are caused more by cytoplasmic protein or membrane networks.
Population
BL6, CD1/J6/129svJ, and Vdac1-deficient murine cardiac myocytes and skeletal myocytes
Comparison
Intact vs membrane-extracted myocytes, cardiac vs skeletal myofilaments, and wild-type vs Vdac1 knockout
Design
Preclinical experimental study using optical and electrical methods
Authors
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Restricts solute diffusion in murine myocytes; leaves open Vdac1 effects on human cardiac energetics.
Both myofilaments and mitochondria networks restrict diffusion in cardiac myocytes, suggesting long-range solute diffusion may preferentially occur via porin channels and intramembrane mitochondrial spaces.
Deisl et al. (2023) studied this question. Vdac1 knockout and molecular weight variations vs. Wild-type myocytes and free water was evaluated on Solute diffusion restriction. Solute diffusion in murine cardiac myocytes is highly restricted by myofilaments and mitochondrial networks, with diffusion being 2.5-fold more restricted in myocytes lacking the mitochondrial porin Vdac1.
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