JNKs belong to mitogen activated protein kinases family and are involved in regulation of various cellular responses including cell survival, cell proliferation and differentiation. They can be activated by several factors such as radiation, stress, growth factors , cytokines and extracellular signals. JNKs activation results in phosphorylation of downstream molecules involve in normal cellular processes. Furthermore the recent data have linked JNK signaling with different pathological coditions, including inflammation, cancer , neurodegenrative disease and cardiac hypertrophy. Gq signaling initiates hypertrophic growth of neonatal rat cultured myocytes and is postulated to transduce in vivo cardiac pressure overload hypertrophy.however with the over expression of c-jun through Ap-1 and ATF-2 transcripting factor, it can cause decompensatory hypertrophy which can proceed to cardiac failure. This review analyzes our present understanding of the role of JNK in apoptotic signaling in heart failure and some other mechanism which induces apoptosis in cardiomyocytes.