主持国家科学自然基金及江苏省科学自然基金等课题6项：1 国家科学自然基金青年基金 (NO.81400300)，水通道蛋白4基因沉默介导的内质网应激途径在心肌肥厚中的作用。23万，2014.1-2017.12，负责人。2 江苏省青年科学自然基金(NO.BK20130642)，信号通路PKCβ-P66Shc-NADPH氧化酶在肾小管上皮细胞损伤中的作用探讨。20万， 2014.6-2017.6，负责人。3 东南大学基础科研扶持项目(NO.2242018K40028)，负责人。4 东南大学基础科研扶持项目(NO.2242017K40092)，负责人。5 东南大学基础科研扶持项目(NO.9224000011)，负责人。6 东南大学新教师科研启动金(NO. 9224000013)，负责人。参与其他国家科学自然基金项目多项：1 国家科学自然基金面上项目(NO.81773796)，ciR-0001544靶向调控ZC3H4在矽肺炎症和纤维化中的作用研究。2 国家科学自然基金青年项目(NO.81600045)，ciR-0000064/LRRC8D通路参与矽肺纤维化的研究。3 国家科学自然基金青年项目(NO.81803182)，ciR-0013395/CollagenI 通路参与二氧化硅诱导的肺内皮间质转化的分子机制研究。以第一作者发表SCI论文多篇，近年来发表文章如下：1. ChengY#, Luo W, Li Z, Cao M, Zhu Z, Han C, Dai X, Zhang W, Wang J, Yao H, ChaoJ#. CircRNA-012091/PPP1R13B-mediated lung fibrotic response in silicosis via ERstress and aautophagy. Am J Resp Cell Mol Biol.2019, 61(3):380-391. (SCI) Article2. ChengYS#, Chao J, Chen C, Lv LL, Han YC, Liu BC*. The PKCβ-p66shc-NADPH oxidasepathway plays a crucial role in diabetic nephropathy. J Pharm Pharmacol. 2019Mar;71(3):338-347. (SCI) Article3. Fang S#, Guo H#, Cheng Y#, Zhou Z, Zhang W, Han B, Luo W, Wang J, Xie W*, Chao J*.circHECTD1 promotes the silica-induced pulmonary endothelial-mesenchymaltransition via HECTD1. Cell Death Dis. 2018 Mar;9(3):396. (SCI) Article4. Cheng Y#, Chao J, Dai D, Dai Y, Zhu D,Liu B*. AQP4-knockout aggravation ofisoprenaline-induced myocardial injury is mediated by p66Shc and endoplasmicreticulum stress. Clin Exp Pharmacol Physiol. 2017 Nov;44(11):1106-1115. (SCI)Article5. ChengYS#, Chao J, Dai DZ*, Dai Y, Zhu DD, LiuBC*. Liuwei dihuang decoction improveddiabetic cardiomyopathy by inhibiting the abnormal expression of theendoplasmic reticulum calcium handling system. Basic & Clinicalpharmacology & Toxicology 2017, 121(Suppl.5),3-40. (SCI) Meeting Abstract6. ChengYS#, Dai DZ, Dai Y, Zhu DD, LiuBC*. Exogenous hydrogen sulphideameliorates diabetic cardiomyopathy in rats by reversing disorderedcalcium-handling system in sarcoplasmic reticulum. J Pharm Pharmacol. 2016Mar;68(3):379-388. (SCI) Article7. Cheng YS#, Dai DZ, Dai Y, Liu BC*. Brain insults caused by intermittent hypoxia due to endoplasmicreticulum stress, activated p66Shc and NADPH oxidase are attenuated byCPU86017-RS compound. WIT Transactions on Biomedicine and Health. 2014,18,111-118. (EI) Conference Article8. ChengYS#, Dai DZ*, Dai Y. AQP4 KO exacerbating renal dysfunction is mediated byendoplasmic reticulum stress and p66Shc and is attenuated by apocynin andendothelin antagonist CPU0213. Eur J Pharmacol. 2013 Dec 5;721(1-3):249-58.(SCI) Article9. Shi FH#, Cheng YS#, Dai DZ*,Peng HJ, Cong XD, Dai Y. Depressed calcium-handling proteins due to endoplasmicreticulum stress and apoptosis in the diabetic heart are attenuated byargirein. Naunyn Schmiedebergs Arch Pharmacol. 2013 Jun;386(6):521-31. (SCI)Article 10. ChengYS#, Cong XD, Dai DZ*, Zhang Y, Dai Y. Argirein alleviates corpuscavernosum dysfunction by suppressing pro-inflammatory factors p66Shc and ERstress chaperone Bip in diabetic rats. J Pharm Pharmacol. 2013Jan;65(1):94-101. (SCI) Article11. ChengYS#, Dai DZ, Dai Y, LiuBC*.Hydrogen sulfide attenuatesdiabetic cardiomyopathy by normalizing ET -NOX-PKC epsilonpathway-in-streptozotocin-injected rats. Acta Pharmacologica Sinica. 2013Aug,34,s8.8. (SCI) Meeting Abstract