Background　Generating protective signals by postconditioning performed in a tissue remote from the target organ such as the limb, i.e. remote postconditioning, is an approach to exerting endogenous tissue protection.　Objective　This review will focus on cardioprotective effect, mechanisms and clinical translation of remote postconditioning.　Content　Remote postconditioning has been observed to reduce myocardial ischemia/reperfusion(I/R) injury experimentally in multiple species, including rat, rabbit and pig. Both tissue necrosis and apoptosis are reduced. As remote preconditioning, remote postconditioning requires a transfer or communication of protective factors or signals through humoral and/or neural pathways. Triggers of target organ protection include G-protein-coupled receptor ligands, metabolites of ischemia, or small thermolabile molecules. Clinical studies investigating improvements in clinical outcomes or biomarkers with remote postconditioning are encouraging.　Trend　Unlike conventional ischemic preconditioning and postconditioning, physiological and molecular mechanisms underlying remote postconditioning are still poorly understood. If further studies show improved clinical outcomes of patients by remote postconditioning, the implications for practice are immense.