Foy et al. use a computer model of muscle ion fluxes to explore why some patients with periodic paralysis develop weakness in conditions of high serum K⁺, while others develop it in conditions of low serum K⁺.

This study reports that the loss of FAT3, a multifunctional tissue polarity protein, acts via its intracellular domain and retinal bipolar cells to affect mouse electroretinography (ERG) responses and visual perception of high-frequency flickers.

We have created a mathematical model to provide a better understanding of the contribution of contractile and regulatory proteins to the regulation of contraction of mammalian cardiac muscle.

Köster et al. characterize eight sodium channel subtypes relevant to nociception and use a computer model to simulate the response of two types of nociceptive nerve fibers. Their results provide a better understanding of Na_v1.7 and Na_v1.9 and have implications for future mechanistic studies and disease modelling.

Elhanafy et al. show that identical mutations at equivalent positions in VSDs of cardiac sodium channels can lead to diverse functional effects. Using molecular dynamics simulations, they uncover VSD-specific structural dynamics and gating-pore conformations that explain these differential impacts, advancing our understanding of sodium channelopathies.

Tao and Corry investigate how the binding of sodium channel inhibitors to the Na_v1.5 pore using simulations reveal promiscuous, polyspecific binding at the fenestrations and central cavity. These findings shed light on diverse ways drugs inhibit the channel, offering insights for improving therapeutic development for conditions like chronic pain, epilepsy, and cardiac arrhythmias.

Apel et al. demonstrate that the calcium-binding protein S100A1 binds the N2A region of titin and that binding is regulated through calcium concentration and pH. Their work suggests that this interaction is a physiological sensor to regulate titin function in the muscle.