Aim To investigate the interaction and mechanism of PARP1 and NFATc3, NFATc4 in ISO-induced pathological cardiac hypertrophy. Methods To establish the model of cardiac hypertrophy in vitro and in vivo, primary neonatal rat cardiomyocytes were treated with ISO (10 jimol • L-1) for 24 h; SD rats were subcutaneously injected with 1. 2 mg • kg-1 • d-1 ISO for 7 d. The nuclear and cytoplasmic proteins were separated by Cellytic Nuclear Extraction Kit. The subcellular localization of NFATc3 and NAFTc4 were detected by Western blot and immunofluorescence. The recombinant adenovirus (Ad-PARPl) infection was used to overexpress PARP1 and knockdown PARP1 by transfecting with siRNA of PARP1 in cardiomyocytes. Results The models of cardiac hypertrophy were successfully built both in vivo and vitro by ISO. It was determined that NFATc3 and NFATc4 were transfered into the nuclear from the cytoplasm in primary neonatal rat cardiomyocytes (NRCMs) after being treated with ISO. And the enzymatic activity of PARP1 was boosted in TSO-trpatpH prmin. OvprpYnrp.ssinn of PARP1 nromo-ted the nuclear translocation of NFATc3 and NFATc4 in cardiomyocytes, while knockdown of PARP1 could reverse the nuclear translocation induced by ISO. PARP1 inhibitor 3AB retarded ISO-induced nuclear transportation of NFATc3 and NFATc4 to some extent. Conclusions ISO leads to the up-regulation of enzymatic activity of PARP1 and promotes nuclear translocation of NFATc3 and NFATc4, thus aggravating car-diac hypertrophy.