<p>Calcium signaling has a fundamental importance in maintaining various platelet functions, such as those involved in hemostasis and thrombosis. Agonist-induced mobilization of calcium (Ca²⁺) 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 Ca²⁺ that contributes to bioenergetics, cytosolic Ca²⁺ buffering, cell signaling and death. Voltage-dependent anion channels (VDAC) in the outer mitochondrial membrane and mitochondrial Ca²⁺ uniporter complex (MCUC) in the inner mitochondrial membrane (IMM) are pivotal for transporting Ca²⁺ into the mitochondrial matrix. On the other hand, matrix Ca²⁺ efflux is dependent on the IMM localized sodium/calcium exchanger (NCLX). Despite the well-established role of cytosolic Ca²⁺, the participation of mitochondrial Ca²⁺ homeostasis in platelet physiology remains unknown. This mini-review summarizes the recent developments in the field of mitochondrial Ca²⁺ transport in platelet physiology.</p>