Calcium signaling has a fundamental importance in maintaining various platelet functions, such as those involved in hemostasis and thrombosis. Agonist-induced mobilization of calcium (Ca ²⁺ ) from intracellular stores coupled with activation of store-operated calcium entry (SOCE) and non-SOCE or receptor-operated calcium entry (ROCE) regulates platelet degranulation, integrin activation, shape change, generation of thromboxane A2, and aggregation or procoagulant function. Platelet mitochondria also take up a small amount of cytosolic Ca ²⁺ that contributes to bioenergetics, cytosolic Ca ²⁺ buffering, cell signaling and death. Voltage-dependent anion channels (VDAC) in the outer mitochondrial membrane and mitochondrial Ca ²⁺ uniporter complex (MCUC) in the inner mitochondrial membrane (IMM) are pivotal for transporting Ca ²⁺ into the mitochondrial matrix. On the other hand, matrix Ca ²⁺ efflux is dependent on the IMM localized sodium/calcium exchanger (NCLX). Despite the well-established role of cytosolic Ca ²⁺ , the participation of mitochondrial Ca ²⁺ homeostasis in platelet physiology remains unknown. This mini-review summarizes the recent developments in the field of mitochondrial Ca ²⁺ transport in platelet physiology.