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Stretch-activated cation channels (SACs), also known as mechanosensitive channels or stretch-gated ion channels, are membrane proteins that open in response to mechanical deformation of the cell membrane, allowing the passage of cations such as Na⁺, K⁺, and sometimes Ca²⁺[1][3]. These channels are found in both prokaryotic and eukaryotic cells, playing important roles in sensing mechanical stimuli such as touch, pressure, stretch, and sound. In animals, SACs participate in mechanotransduction required for touch, hearing, balance, and proprioception, and they regulate cell volume and the response to osmotic stress[1][3][5]. Several structural families exist, including the TREK and TRAAK channels (potassium-selective), DEG/ENaC (sodium-selective), and others involved in both sensory and homeostatic processes[1]. Some SACs are pharmacologically modulated, notably suppressed by gadolinium ions, which has helped to delineate their physiological functions[4]. Dysfunction or dysregulation of these channels has been implicated in cardiovascular, neurodegenerative, auditory, and pain disorders[6].
Inhibition of ion flux by blocking or modulating channel opening (e.g., gadolinium reduces or blocks cation flow in response to stretch)
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