Speaker Bio

Dr. Quan CHEN is the Dean of the College of Life Sciences, Nankai University, and the Director of the State Key Laboratory of Medicinal Chemical Biology. He obtained his Ph.D. from the Chinese Academy of Sciences and received his post-doctoral training in Manchester University, UK and in the Cleveland Clinic Foundation, Ohio, USA before returning to China to establish his own laboratory in the year 2000. Dr. Chen has previously served as the Director of the State Key Laboratory of Membrane Biology. He was elected as an executive member of the Chinese Society of Biophysics and the Chinese Society of Cell Biology, and as Director of the Society of Membrane Biology in the Chinese Society of Biophysics. He is the Editor-in-Chief of the newly launched journal Mitochondrial Communications, and currently serves as an editorial board member for FEBS Letters, Cell Research, JBC, Cell Death & Disease, Open Biology, JCMM, and several Chinese national journals. He also serves as Vice President of the Asian Society of Mitochondrial Research and Medicine.

The research in Dr. Chen’s laboratory is focused on the molecular regulation of mitochondrial dynamics and mitochondrial quality control. In particular, his laboratory has identified a new mitophagy receptor, FUNDC1, that mediates mitophagy and regulates mitochondrial homeostasis. He seeks to understand how defective mitophagy is linked to aging and aging-related diseases such as metabolic disorders, neurodegenerative diseases, and cancers.

陈佺，国家级领军人才，国家自然科学基金委杰出青年基金获得者。1993年获得中国科学院动物研究所博士学位，1994-2002年分别于英国曼彻斯特大学和美国俄亥俄州克利夫兰医学基金会勒内研究所肿瘤生物学室从事博士后研究，2001-2006年，担任生物膜与膜生物工程国家重点实验室主任，2019年开始任南开大学生命科学学院院长、药物化学生物学国家重点实验室主任。

陈佺教授集中研究线粒体在细胞凋亡调控中的关键作用和线粒体自吞噬的分子调节，线粒体功能异常在神经退行性疾病如老年痴呆和帕金森综合症发生中的关键作用，探讨肿瘤干细胞在肿瘤发生和肿瘤转移中的关键作用。先后主持国家自然科学基金委重点项目、重大计划集成项目、科学院知识创新工程先导项目、国家科技部973项目和科技创新项目等。研究成果发表在Nature Communications， Cell Research等权威杂志。陈佺教授曾获美国癌症研究学会(AACR-AFLAC)癌症研究青年学者奖、第四届谈家桢生命科学奖创新奖、全国优秀科技工作者等荣誉称号。

Abstract

Mitochondria are highly dynamic and undergo constant turnover through two opposing processes: mitophagy, which selectively removes superfluous and damaged mitochondria by the autolysosomal pathway, and mitochondrial biogenesis, which generates fresh, functional ones. We have previously revealed that FUNDC1, a mitochondrial outer-membrane protein, functions as a mitophagy receptor to mediate hypoxia-induced mitophagy. FUNDC1 harbors an LC-3–interacting region (LIR) and interacts with LC-3 to mediate mitophagy. Interestingly, we found that PGC-1α and NRF1, master regulators of mitochondrial biogenesis and metabolic adaptation, also transcriptionally up-regulate Fundc1 in response to cold stress in brown fat tissue (BAT). Our results demonstrate that FUNDC1-dependent mitophagy is directly coupled with mitochondrial biogenesis through the PGC-1α/NRF1 pathway, which dictates mitochondrial quantity, quality and turnover and contributes to adaptive thermogenesis. I will also introduce that abnormal mitochondrial homeostasis contributes to cellular senescence and aging-associated diseases.