Resting Ca²⁺ fluxes protect cells from fast mitochondrial fragmentation, cell stress responses, and immediate transcriptional reprogramming.

ABSTRACT: Homeostatic calcium ion (Ca²⁺) fluxes between the endoplasmic reticulum, cytosol, and extracellular space occur not only in response to cell stimulation but also in unstimulated cells. Using murine astrocytes as a model, we asked whether there is a signaling function of these resting Ca²⁺ fluxes. The data showed that endoplasmic reticulum (ER) Ca²⁺ depletion, induced by sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase (SERCA) inhibition, resulted to prolonged Ca²⁺ influx and mitochondrial fragmentation within 10 to 30 min. This mitochondrial fragmentation could be prevented in Ca²⁺-free medium or by inhibiting store-operated Ca²⁺ entry (SOCE). Similarly, attenuation of STIM proteins, which are vital ER Ca²⁺ sensors, protected mitochondri

SUBMITTER: Fecher C 

PROVIDER: S-EPMC12167414 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature