Mitochondria are critical organelles of energy metabolish and signal transduction in eukaryotes. Mitochondrial dysfunction leads to impaired ATP generation and structural alterations of the respiratory chain

which closely relates to the development and progression of many diseases. Heat shock protein 22(HSP22)is a member of the superfamily of small heat shock proteins. HSP22

upregulated by various conditions of mammalian myocardial stress

such as ischemia and cardiac overload

plays a critical role of promoting myocardial survival and maintaining myocardial function. Therefore

HSP22 may be a new potential treatment of diseases whose etiology is based upon dysfunction of mitochondria. Meanwhile

HSP22 may play a vital role in slowing down cardiac aging. We review the cardioprotection of HSP22 under physiological and pathological conditions from mitochondrial protection perspective.