李奇，1993年12月出生，中共党员，医学博士，主治医师，硕士生导师，“湖北省青年科技人才晨光托举工程”入选者，宜昌市中心人民医院高层次科技拔尖人才，主要从事缺血性心脏病的基础及临床研究。主持国家自然科学基金1项、湖北省自然科学基金1项，湖北省卫生健康科技项目1项以及宜昌市科技计划项目1项。以第一作者（含共一）发表SCI论文10余篇，单篇最高影响因子38.6，研究成果获得湖北省科技进步奖一等奖1项。
联系方式：liqi@ctgu.edu.cn
近五年代表性论文：
1. Li Q, He G, Zheng R, Liu C, Wang C, Liu Z, Li Z, Lu C. Ferroptosis-related Biotargets and Network Mechanisms of Maslinic Acid Against Myocardial Ischemia-reperfusion Injury: An Integrated Bioinformatic and Experimental Approach. Comb Chem High Throughput Screen. 2025 Jan 2.
2. Li Q, Li Z, Liu C, et al. Maslinic Acid Ameliorates Myocardial Ischemia Reperfusion Injury-Induced Oxidative Stress via Activating Nrf2 and Inhibiting NF-κB Pathways. Am J Chin Med. 2023.
3. Li Q, Li Z, Lu C. Letter by Li et al Regarding Article, "Circulating MicroRNA-122-5p Is Associated With a Lack of Improvement in Left Ventricular Function After Transcatheter Aortic Valve Replacement and Regulates Viability of Cardiomyocytes Through Extracellular Vesicles". Circulation. 2023; 147(4):e66-e67.
4. Li Q, Zhao L, Wang C, et al. Loganin: A potential pharmacological agent for myocardial ischemia- reperfusion injury. Int J Cardiol. 2023, 10:131650.
5. Li Q, Xu M, Li Z, Li T, Wang Y, Chen Q, Wang Y, Feng J, Yin X, Lu C. Maslinic Acid Attenuates Ischemia/Reperfusion Injury-Induced Myocardial Inflammation and Apoptosis by Regulating HMGB1-TLR4 Axis. Front Cardiovasc Med. 2021, 8:768947.
6. Li Q, Li Z, Li T, et al. Involvement of the crosstalk between Nrf2 and NF-κB pathways regulated by SIRT1 in myocardial ischemia/reperfusion injury. Int J Cardiol. 2022, 355:44.
7. Li Q, Li Z, Li T, et al. Efficacy and safety of soluble guanylate cyclase stimulators in patients with heart failure: A systematic review and meta-analysis. Pharmazie. 2021, 76(10):488-493.
8. Li Q, Li Z, Fan Z, et al. Involvement of non‑coding RNAs in the pathogenesis of myocardial ischemia/reperfusion injury (Review). Int J Mol Med. 2021, 47(4):42.
9. Li Q, Yang J, Zhang J, et al. Inhibition of microRNA-327 ameliorates ischemia/reperfusion injury-induced cardiomyocytes apoptosis through targeting apoptosis repressor with caspase recruitment domain. J Cell Physiol. 2020, 235(4):3753-3767.
