Figure 1.

Schematic representation illustrating the hypothesis. During sepsis, Drp1 is recruited from the cytosol into the mitochondrial outer membrane and forms oligomers to divide a single mitochondrion into two separated mitochondria, which is termed mitochondrial fission. Enhanced mitochondrial fragmentation could lead to mitochondrial dysfunction, which induces ER stress. Interestingly, mitochondrial fission induces ER stress by, at least partly, overproduction of ROS. Therefore, we hypothesized that Mdivi-1, a selective inhibitor of Drp1, protects CD4⁺ T cells against apoptosis and is probably through reestablishing the mitochondrial fusion-fission balance and preventing the induction of ER stress. Moreover, ROS was a potential connection between mitochondrial dynamics and ER stress.