Reggiani Carlo, Marcucci Lorenzo
Department of Biomedical Sciences, University of Padova, Via Marzolo 3, 35131, Padova, Italy.
ZRS, Science and Research Center, Garibaldijeva 1, 6000, Koper, Slovenia.
Pflugers Arch. 2025 Oct;477(10):1241-1243. doi: 10.1007/s00424-025-03120-5. Epub 2025 Sep 20.
In muscle fibers, unloading and disuse cause an increase in resting calcium concentrations in the cytosol and mitochondrial matrix. S107, a stabilizer of the Ryanodine Receptor calcium channel (RyR), blocks the leakage from the sarcoplasmic reticulum and lowers mitochondrial calcium concentrations without altering cytosolic calcium levels, as demonstrated in a recent article published in Pflugers Archives (Sidorenko et al. 2025). This finding is important as it shows that, even at rest, calcium entry into the mitochondria is influenced by RyR leakage, thanks to the mitochondria unique location near the sarcoplasmic reticulum membranes. Given the role of mitochondrial function in controlling muscle fiber size, these findings may have a significant translational relevance in the treatment of disuse-induced atrophy.
在肌纤维中，卸载和废用会导致细胞质和线粒体基质中静息钙浓度升高。如最近发表在《普弗卢格氏文献》（Sidorenko等人，2025年）上的一篇文章所示，兰尼碱受体钙通道（RyR）的稳定剂S107可阻止肌浆网的钙泄漏，并降低线粒体钙浓度，而不改变细胞质钙水平。这一发现很重要，因为它表明，即使在静息状态下，由于线粒体位于肌浆网膜附近的独特位置，进入线粒体的钙也会受到RyR泄漏的影响。鉴于线粒体功能在控制肌纤维大小方面的作用，这些发现可能在废用性萎缩的治疗中具有重要的转化意义。
