Mingjie Gao, Weiyi Hu, Delan Meng, Pengju Yao, Siqi Yang, Yuanpeng Tong, Lei Wang, Ya Zhang, Qingsong Wang, Jianguo Ji, Wenyuan Zhu
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引用次数: 0
摘要
线粒体自噬功能失调导致受损线粒体的病理性积累,与癌症、阿尔茨海默病等人类疾病的发生发展密切相关。鉴定更安全、更有效的线粒体自噬调节因子可能为治疗线粒体疾病提供新的途径。共价结合药物因其高特异性、选择性和低耐药潜力而受到广泛关注。在这项研究中,我们证明了天然环氧化合物jolkinolide B (JB)在体外和体内都能特异性诱导线粒体自噬。质谱分析证实,JB直接结合线粒体外膜转位酶蛋白TOM40,导致胰腺癌自噬细胞死亡。作为一种线粒体自噬增强剂,JB还可以改善5×FAD阿尔茨海默病小鼠模型中的线粒体功能障碍和认知缺陷。研究结果表明,JB选择性地靶向线粒体以增强线粒体自噬,同时在胰腺癌和阿尔茨海默病小鼠模型中表现出最小的毒性,突出了其作为线粒体疾病治疗剂的潜力。
Jolkinolide B Activates Mitophagy to Exhibit Antipancreatic Cancer Activity and Alleviate Cognitive Deficits in Alzheimer's Disease.
Dysfunctional mitophagy leads to the pathological accumulation of damaged mitochondria, which is closely associated with the development of human diseases such as cancer and Alzheimer's disease. The identification of safer and more effective mitophagy regulators may provide a novel approach for treating mitochondrial diseases. Covalent-binding drugs have attracted substantial attention due to their high specificity, selectivity, and low resistance potential. In this study, we demonstrated that the natural epoxide compound jolkinolide B (JB) specifically induces mitophagy both in vitro and in vivo. Mass spectrometry analysis confirmed that JB directly binds to the outer mitochondrial membrane translocase protein TOM40, leading to autophagic cell death in pancreatic cancer. As a mitophagy enhancer, JB also ameliorates mitochondrial dysfunction and mitigates cognitive deficits in the 5×FAD mouse model of Alzheimer's disease. The findings indicate that JB selectively targets mitochondria to enhance mitophagy while exhibiting minimal toxicity in pancreatic cancer and Alzheimer's disease mouse models, highlighting its potential as a therapeutic agent for mitochondrial diseases.
期刊介绍:
The mission of MCP is to foster the development and applications of proteomics in both basic and translational research. MCP will publish manuscripts that report significant new biological or clinical discoveries underpinned by proteomic observations across all kingdoms of life. Manuscripts must define the biological roles played by the proteins investigated or their mechanisms of action.
The journal also emphasizes articles that describe innovative new computational methods and technological advancements that will enable future discoveries. Manuscripts describing such approaches do not have to include a solution to a biological problem, but must demonstrate that the technology works as described, is reproducible and is appropriate to uncover yet unknown protein/proteome function or properties using relevant model systems or publicly available data.
Scope:
-Fundamental studies in biology, including integrative "omics" studies, that provide mechanistic insights
-Novel experimental and computational technologies
-Proteogenomic data integration and analysis that enable greater understanding of physiology and disease processes
-Pathway and network analyses of signaling that focus on the roles of post-translational modifications
-Studies of proteome dynamics and quality controls, and their roles in disease
-Studies of evolutionary processes effecting proteome dynamics, quality and regulation
-Chemical proteomics, including mechanisms of drug action
-Proteomics of the immune system and antigen presentation/recognition
-Microbiome proteomics, host-microbe and host-pathogen interactions, and their roles in health and disease
-Clinical and translational studies of human diseases
-Metabolomics to understand functional connections between genes, proteins and phenotypes