Mitochondria are metabolic centers within cells, possessing their own genetic materials independent of the cell nucleus. They play a crucial role in maintaining cellular homeostasis and individual health through biogenesis, fusion, division, autophagy and mitochondrial protease regulation. Mitochondria also act as hubs for cell death, autophagy, innate immunity, biosynthesis, cellular metabolism and cell signaling. Mitochondrial dysfunction and mtDNA mutations are closely related to the occurrence of neurodegenerative diseases, cardiovascular diseases, metabolic disorders and tumors, posing significant threats to human health.

This session will discuss new techniques and methods in mitochondrial research, as well as new mechanisms underlying mitochondrial dysfunction in the development of human diseases. 

Chairs

Song Zhiyin

Professor, Wuhan University

Zhu Yushan

Professor, Nankai University 

Invited speakers & reports

Shi Yunyu

University of Science and Technology of China 

Report: Mitochondrial epigenetic regulation and human degenerative diseases

Guan Minxin

Professor, Zhejiang University

Report: Mitochondrial gene mutations regulate mitochondrial quality control and apoptosis 

Qi Bin

Yunnan University

Report: Bacterial peptidoglycan activates food digestion through inhibiting the mitochondrial unfolded protein response

Chen Liangyi

Professor, Peking University

Report: Super-resolution imaging determines the structure and mitochondrial phenotype of tau pathology 

Pan Xin

Research fellow, Academy of Military Medical Sciences

Report: Mitochondrial abnormalities and diseases 

Jiang Hui

Research fellow, National Institute of Biological Sciences, Beijing

Report: Mitochondrial autophagy regulation and diseases 

Liu Lei

Research fellow, Institute of Zoology, Chinese Academy of Sciences

Report: Mitochondria and ferroptosis

Gan Zhenji

Professor, Nanjing University

Report: Mitochondrial metabolism and homeostasis

Long Qi

Guangzhou Institute of Biomedicine and Health, CAS

Report: TCA enzymes act as messengers from mitochondria to the nucleus