Personal Profile

Liang Sijia, Professor, Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University. He obtained her Ph.D. in Pharmacology from Sun Yat-sen University in 2014. From 2015 to 2021, he carried out research work as a postdoctoral fellow/specially-appointed researcher at the Zhongshan School of Medicine. He is a member and deputy secretary-general of the Cardiovascular Pharmacology Professional Committee of the Chinese Pharmacological Society, and the deputy director of the Young Committee of Cardiovascular Pharmacology of the Chinese Pharmacological Society. He is dedicated to the research on the pathogenic mechanisms of metabolic cardiovascular diseases, especially those induced by hyperlipidemia, and systematically studies the pathological significance of calcium store-operated calcium channels and calcium-activated chloride channels in the cardiovascular system in diseases. In recent years, as the first author or corresponding author, he has published many papers in journals such as European Heart Journal, Advanced Science, and Arteriosclerosis, Thrombosis, and Vascular Biology. He has presided over multiple National Natural Science Foundation projects and provincial-level projects.

Academic Achievements

Representative Publications

• Liu X#, Guo JW#, Lin XC#, Tuo YH#, Peng WL#, He SY, Li ZQ, Ye YC, Yu J, Zhang FR, Ma MM, Shang JY, Lv XF, Zhou AD, Ouyang Y, Wang C, Pang RP, Sun JX, Ou JS*, Zhou JG*, Liang SJ*. Macrophage NFATc3 prevents foam cell formation and atherosclerosis: evidence and mechanisms. European Heart Journal. 2021, 14;42(47):4847-4861. (IF = 29.98)
• Guo JW#, Liu X#, Zhang TT#, Lin XC#, Hong Y, Yu J, Wu QY, Zhang FR, Wu QQ, Shang JY, Lv XF, Ou JS, Zhou JG, Pang RP*, Tang BD*, Liang SJ*. Hepatocyte TMEM16A deletion retards NAFLD progression by ameliorating hepatic glucose metabolic disorder. Advanced Science. 2020, 7(10):1903657. (IF = 16.806)
• Lv XF#, Zhang YJ#, Liu X#, Zheng HQ#, Liu CZ, Zeng XL, Li XY, Lin XC, Lin CX, Ma MM, Zhang FR, Shang JY, Zhou JG, Liang SJ*, Guan YY*. TMEM16A ameliorates vascular remodeling by suppressing autophagy via inhibiting Bcl-2–p62 complex formation. Theranostics. 2020, 10(9):3980-3993. (IF = 11.556)
• Liang SJ#, Zeng DY#, Mai XY#, Shang JY#, Wu QQ, Yuan JN, Yu BX, Zhou P, Zhang FR, Liu YY, Lv XF, Liu J, Ou JS, Qian JS*, Zhou JG*. Inhibition of Orai1 store-operated calcium channel prevents foam cell formation and atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 2016, 36(4):618-628. (IF = 8.311)
• Liu YY#, Liu X, Zhou JG, Liang SJ*. MicroRNA-302a promotes neointimal formation following carotid artery injury in mice by targeting PHLPP2 thus increasing Akt signaling. Acta Pharmacologica Sinica. 2021,42(4):550-559. (IF = 6.15)
• Li K#, Liu YY#, Lv XF#, Lin ZM, Zhang TT, Zhang FR, Guo JW, Hong Y, Liu X, Lin XC, Zhou JG, Wu QQ, Liang SJ*, Shang JY*. Reduced intracellular chloride concentration impairs angiogenesis by inhibiting oxidative stress-mediated VEGFR2 activation. Acta Pharmacologica Sinica. 2021,42(4):560-572 (IF = 6.15)
• Tang BD#, Xia X#, Lv XF#, Yu BX, Yuan JN, Mai XY, Shang JY, Zhou JG, Liang SJ*, Pang RP*. Inhibition of Orai1-mediated Ca²⁺ entry enhances chemosensitivity of HepG2 hepatocarcinoma cells to 5-fluorouracil. Journal of Cellular and Molecular Medicine. 2017, 21(5):904-915. (IF = 5.31)
• Mai XY#, Shang JY#, Liang SJ#, Yu BX, Yuan JN, Lin Y, Luo RF, Zhang FR, Liu YY, Lv XF, Li CL, Liang XL, Wang WD*, Zhou JG*. Blockade of Orai1 store-operated calcium entry protects against renal fibrosis. Journal of the American Society of Nephrology. 2016, 27(10):3063-3078. (IF = 10.121)
• Huang LY#, He Q#, Liang SJ#, Su YX#, Xiong LX, Wu QQ, Wu QY, Tao J, Wang JP, Tang YB, Lv XF, Liu J, Guan YY, Pang RP*, Zhou JG*. ClC-3 defect contributes to inflammatory bowel disease in humans and mice. Gut. 2014, 63(10):1587-95. (IF = 23.059)

Research Projects

1. National Natural Science Foundation of China, General Project, 82073839. Research on the mechanism by which PCDH7 downregulation promotes the formation of aortic dissection by inducing phenotypic transformation of vascular smooth muscle cells. From January 2021 to December 2024, with a fund of 560,000 yuan. Ongoing.
2. National Natural Science Foundation of China, General Project, 81773723. Research on the mechanism by which the Ca²⁺-Calcineurin-NFAT4 signaling inhibits macrophage foam cell formation and atherosclerosis. From January 2018 to December 2021, with a fund of 550,000 yuan. Ongoing.
3. National Natural Science Foundation of China, Youth Project, 81603098. Research on the mechanism by which Endophilin A2 improves ischemic myocardial injury by promoting angiogenesis. From January 2017 to December 2019, with a fund of 173,000 yuan. Completed.
4. Guangdong Provincial Natural Science Foundation, Doctoral Startup Project, 2014A030310031. Research on the mechanism by which Endophilin A2 regulates eNOS and endothelial diastolic dysfunction. From January 2015 to January 2018, with a fund of 100,000 yuan. Completed.
5. Guangzhou Science and Technology Plan Project, General Project, 201707010023. Research on the molecular mechanism by which Endophilin A2 regulates VEGFR2 activity to improve ischemic myocardial injury. From May 2017 to April 2020, with a fund of 200,000 yuan. Completed.