细胞死亡与疾病。Cell death and Diseases

我们主要研究坏死性细胞凋亡的分子机制及其在包括肿瘤等炎症相关性疾病中的作用。同时，我们课题组也致力于新型抗坏死性细胞凋亡药物发现与转化应用研究。坏死性凋亡与不可调控性细胞坏死表现相似的形态学特征，包括细胞肿胀、细胞膜破裂和细胞内容物释放等。由于细胞内容物的释放，坏死性细胞凋亡会引起体内大量炎症细胞浸润从而诱发严重的炎症反应。目前的研究表明，坏死性细胞凋亡作为新的一类细胞程序性死亡方式，在缺血性损伤、神经退行性疾病、恶性肿瘤、病毒感染和免疫性疾病等多种疾病的病理生理过程中起重要作用，发现其小分子抑制剂对于坏死性凋亡相关疾病的临床治疗具有十分重大的意义。

本课题组主要研究方向：

（1）抗坏死性凋亡小分子药物筛选、鉴定与临床应用

（2）坏死性凋亡及其所诱发的炎症反应与肿瘤发生发展的关系（主要以乳腺癌、肝癌和结肠癌为肿瘤模型）；

（3）坏死性凋亡的分子调控机理。

Dr. Cai’s research has been focused on investigating the molecular mechanisms of necroptosis, as well as the necroptotsis related cancer and inflammatory diseases. At the same time, our research group is also committed to the discovery and transformation of new anti-necroptosis drugs.

1.《现代生物医学进展》杂志编委；2.《肿瘤药学》杂志编委；3.美国癌症研究学会会员；4.美国细胞生物学学会会员

2010年于美国德州农工大学健康科学中心获生物医学专业博士学位。

2011年2月至2017年2月在美国国立卫生研究院国立癌症研究所做访问学者，其主要从事坏死性凋亡的分子机制及其相关肿瘤和炎症性疾病的研究。

获得国家自然科学基金及上海市科委等项目资助。近五年来，研究成果以通讯作者或第一作者发表在Nat Cell Biol, Cell Research，PNAS, Cancer Research, Br J Pharmacol, J Med Chem等杂志。其中2篇的研究论文入选ESI前1%高被引论文。申报国内专利2项。

Dr. Cai received his B.S. (2003) and M.S. (2006) degrees from Hunan Normal University. Then, he went to U.S. and earned his Ph.D degree (2010) in biomedical sciences at Texas A&M University Health Science Center. After graduation, he went to National Cancer Institute（NCI, NIH）and worked as a visiting scholar from Feb. 2011 to Feb. 2017. In June.2020, Dr. Cai joined in Tongji University School of Medicine as a professor.

Dr. Cai’s research has been focused on investigating the molecular mechanisms of necroptosis, as well as the necroptosis related cancer and inflammatory diseases. In recent 5 years, Dr. Cai has published several articles in high-profile scientific journals including Nat Cell Biol, Cell Res, PNAS, Cancer Res，Br J Pharmacol and J Med Chem. Two of his articles published in Nat Cell Biol and PNAS were selected as a high-cited paper in Web of Science Database. Dr. Cai has declared two Chinese patent. Dr. Cai’s research was supported from the National Natural Science Foundation of China.

1.Qin X, Hu L, Shi SN, Chen X, Zhuang C, Zhang W, Jitkaew S, Pang X, Yu J, Tan YX#, Wang HY, Cai Z. The Bcr-Abl inhibitor GNF-7 inhibits necroptosis and ameliorates acute kidney injury by targeting RIPK1 and RIPK3 kinases. 2020，Biochem Pharmacol. 177:113947；

2.Qin X, Ma D, Tan Y, Wang H, Cai Z. The role of necroptosis in cancer: a double-edged sword? 2019, Biochim Biophys Acta Rev Cancer, 1871:259-266. (Review)；

3.Chen X, Zhuang C, Ren Y, Zhang H, Qin X, Hu L, Fu J, Miao Z, Chai Y, Liu Z, Wang H , Cai Z. Identification of TAK-632 and its analogues as potent inhibitors of necroptosis by targeting RIPK1 and RIPK3, 2019, Br J Pharmacol, 176(12):2095-2108；

4.Cai Z, Zhang A, Choksi S, Li W, Li T, Zhang X, and Liu Z. Activation of cell surface proteases promotes necroptosis, inflammation and cell migration. 2016, Cell Research, 26(8):886-900；

5.Cai Z, Jitkaew S, Zhao J, Chiang H, Choksi S, Liu J, Ward E, Wu L, Liu Z. Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis. Nat Cell Biol. 2014; 16(1):55-65；

6.Zhao J†, Jitkaew S†, Cai Z†, Choksi S, Li Q, Luo J, Liu ZG. Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosis. Proc Natl Acad Sci U S A. 2012; 109(14):5322-7. (†, equal contribution)