The major developmental significance of leaf senescence is the massive recycling of nutrients from senescing leaves to nascent organs, including seeds, to meet the requirement of their rapid development, so-called nutrient remobilization. The efficiency of nutrient remobilization is associated with the activity of diverse transporters. A large number of transporters are up-regulated during leaf senescence in Arabidopsis, many of which participate in regulating leaf senescence via different signaling pathways. Here, we report that a member of the cation/Ca2+ exchanger family, CCX1, is highly induced during leaf senescence in Arabidopsis. Although single mutation of CCX1 did not change the senescence phenotype, double mutation of CCX1 and CCX4 resulted in a subtle but significant stay-green phenotype during natural and dark-induced leaf senescence, suggesting that some members of the cation/Ca2+ exchanger family act redundantly in mediating leaf senescence. Consistently, overexpression of CCX1 accelerated leaf senescence. Moreover, the ccx1ccx4 double mutant was more tolerant to H2O2, whereas CCX1-overexpressing lines showed an elevated response to H2O2 treatment, presumably due to an overaccumulation of reactive oxygen species (ROS), indicating that CCX1 may promote leaf senescence via modulating ROS homeostasis. Notably, both ccx1-1 and ccx1ccx4 were sensitive to Ca2+ deprivation, implying that CCX1 may also be involved in modulating Ca2+ signaling and consequently affecting the initiation of leaf senescence.