{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,20]],"date-time":"2025-09-20T18:52:37Z","timestamp":1758394357082},"reference-count":30,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2017,7,26]],"date-time":"2017-07-26T00:00:00Z","timestamp":1501027200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label \/><jats:p>Farnesyl pyrophosphate synthase (FPPS) is a key enzyme in the mevalonate pathway. Our previous studies have indicated that cardiac\u2010specific overexpression of FPPS induces cardiac hypertrophy and dysfunction in mice, and inhibition of FPPS prevents angiotensin (Ang) II\u2010induced hypertrophy in cardiomyocytes. However, the role for FPPS in myocardial ischemia\/reperfusion (MIR) injury is still not clear. The objective of this work was to investigate the effect of FPPS on MIR injury in H9c2 cells which were subjected to hypoxia\/reoxygenation (HR) to mimic MIR. Prior to HR, cells were transfected with pE\u2010mFPPS, shFPPS, or pE\u2010GFP. Our results showed that the overexpression of FPPS reduced cell proliferation, increased cell injury and cell apoptosis, and knock\u2010down of FPPS improved cell proliferation, decreased cell injury, and cell apoptosis after HR. Besides, overexpression of FPPS increased Rac1 activity and reactive oxygen species (ROS) generation, while FPPS silencing decreased Rac1 activity and ROS generation. Based on these findings, we propose that knock\u2010down of FPPS reduces Rac1 activity and ROS production, and finally leads to the decrease of HR\u2010induced injury in H9c2 cells. These findings point that FPPS might be a potential target in preventing H9c2 cells from HR\u2010induced injury.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.10795","type":"journal-article","created":{"date-parts":[[2017,5,25]],"date-time":"2017-05-25T16:18:19Z","timestamp":1495729099000},"page":"982-990","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Knock\u2010down of farnesyl pyrophosphate synthase protects heart\u2010derived H9c2 cells against hypoxia\/reoxygenation\u2010induced injury"],"prefix":"10.1002","volume":"41","author":[{"given":"Dongpu","family":"Dai","sequence":"first","affiliation":[{"name":"Institute of Cardiology College of Medicine The First Affiliated Hospital Zhejiang University Hangzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huandong","family":"Wu","sequence":"additional","affiliation":[{"name":"Institute of Cardiology College of Medicine The First Affiliated 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