Shi, JingBei, YihuaKong, XiangqingLiu, XiaojunLei, ZhiyongXu, TianzhaoWang, HuiXuan, QinkaoChen, PingXu, JiahongChe, LinLiu, HuiZhong, JiuchangSluijter, Joost PGLi, XinliRosenzweig, AnthonyXiao, Junjie2017-04-062017Shi, J., Y. Bei, X. Kong, X. Liu, Z. Lei, T. Xu, H. Wang, et al. 2017. “miR-17-3p Contributes to Exercise-Induced Cardiac Growth and Protects against Myocardial Ischemia-Reperfusion Injury.” Theranostics 7 (3): 664-676. doi:10.7150/thno.15162. http://dx.doi.org/10.7150/thno.15162.http://nrs.harvard.edu/urn-3:HUL.InstRepos:32072031Limited microRNAs (miRNAs, miRs) have been reported to be necessary for exercise-induced cardiac growth and essential for protection against pathological cardiac remodeling. Here we determined members of the miR-17-92 cluster and their passenger miRNAs expressions in two distinct murine exercise models and found that miR-17-3p was increased in both. miR-17-3p promoted cardiomyocyte hypertrophy, proliferation, and survival. TIMP-3 was identified as a direct target gene of miR-17-3p whereas PTEN was indirectly inhibited by miR-17-3p. Inhibition of miR-17-3p in vivo attenuated exercise-induced cardiac growth including cardiomyocyte hypertrophy and expression of markers of myocyte proliferation. Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. Collectively, these data suggest that miR-17-3p contributes to exercise-induced cardiac growth and protects against adverse ventricular remodeling. miR-17-3p may represent a novel therapeutic target to promote functional recovery after cardiac ischemia/reperfusion.en-USExerciseCardiac growthmicroRNA.Journal Article2017-04-0610.7150/thno.15162