2025 10th International Conference on Health, Medicine and Life Sciences

Dr. Jun Ren, Professor

Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai, China

Biography:  Dr. Jun Ren is a professor in Department of Cardiology at Zhongshan Hospital Fudan University. He held full professorship in University of Wyoming and University of Washington between 2002 and 2023. His major area of research is cardiac pathophysiology in alcoholism, diabetes, obesity and aging. His research was funded by the National Science Foundation of China, American Diabetes Association and NIH (33+ million). He is a first or corresponding author of more than 700 peer-reviewed papers (H index=120). Ranks among the top 400 in the cardiovascular field globally. He has served as an editor or on editorial board for a number of journals including Science Bulletin, Hypertension, Diabetes, BBA Molecular Basis of Disease.

Topic: Dynamic Regulation and Intervention of Aberrant Mitochondria-Endoplasmic Reticulum Interaction and Metabolic Reprogramming in Heart Failure

Abstract: Heart failure (HF) becomes one of the leading causes of death, with rising incidence and mortality rates. Increasing evidence suggests that changes in myocardial cell metabolism play a central role in the pathogenesis of HF. Under normal conditions, the heart efficiently generates energy through fatty acid oxidation to maintain stable and continuous pumping function. However, in HF, this balance is disrupted, and the heart shifts from fatty acid oxidation to glycolysis for energy production. Although glycolysis rapidly produces ATP in the short term, its efficiency is much lower than that of fatty acid oxidation, leading to a loss of metabolic flexibility. This metabolic disturbance worsens cardiac function, creating a vicious cycle. Despite advancements in HF research, little is known about the deeper molecular mechanisms underlying metabolic reprogramming, particularly the synergistic effects of mitochondrial-endoplasmic reticulum (MAM) interaction abnormalities and glucose-lipid metabolic reprogramming. Both mitochondria and the endoplasmic reticulum are essential for cellular energy production and lipid/protein synthesis, and their interaction plays a key role in HF-associated metabolic alterations. Investigating this complex regulatory network is crucial for understanding HF pathogenesis and developing effective therapeutic strategies.

Dr. Jialiu Wei, Associate Researcher

Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing, China

Biography:  Dr. Jialiu Wei, Associate Researcher, serves as a Youth Committee Member of the Immunotoxicology Committee of the Chinese Society of Toxicology, Deputy Secretary-General of the Science Popularization Committee of the Beijing Environmental Mutagen Society, and holds editorial positions as a Youth Editorial Board Member for Journal of Geriatric Cardiology, Medicine Advances, and Chinese General Practice, as well as a Special Reviewer for Safety, Health & Environment. He focuses on the health effects and mechanisms of environmental pollutants on the cardiovascular and cerebrovascular systems. He has published over 30 SCI papers, such as Journal of Hazardous Materials, Environmental Pollution, and Science of the Total Environment.

Topic: Fat Mass and Obesity-Associated Gene (FTO) Hypermethylation Induced by Decabromodiphenyl Ethane Causing Cardiac Dysfunction via Glucolipid Metabolism Disorder

Abstract: Decabromodiphenyl ethane (DBDPE) is a major alternative to BDE-209 owing to its lower toxicity. However, the mass production and increased consumption of DBDPE in recent years have raised concerns related to its adverse health effects. In the present study, we investigated the impacts of DBDPE on the cardiovascular system in male SD rats and then explored the underlying mechanisms to explain the cardiotoxicity of DBDPE using AC16 cells. Histopathological analysis demonstrated that DBDPE induced cardiomyocyte injury and fibrosis, and ultrastructural observation revealed that DBDPE could induce mitochondria damage and dissolution. DBDPE could thus decrease the level of MYH6 and increase the level of SERCA2, which are the two key proteins involved in the maintenance of homeostasis during myocardial contractile and diastolic processes. In addition, DBDPE could activate the PI3K/AKT/GLUT2 and PPARγ/RXRα signaling pathways in AC16 cells. Bisulfite sequencing PCR (BSP) identified the hypermethylation status of fat mass and obesity-associated gene (FTO). 5-aza exerted the opposite effects on the PI3K/AKT/GLUT2, PPARγ/RXRα, and Cytochrome C/Caspase-9/Caspase-3 signaling pathways induced by DBDPE in AC16 cells. In addition, the DBDPE-treated altered levels of UCP2, ATP, and apoptosis were also found to be significantly reversed by 5-aza in AC16 cells. These results suggested that FTO hypermethylation played a regulative role in the pathological process of DBDPE-induced glycolipid metabolism disorder, thereby contributing to the dysfunction of myocardial contraction and relaxation through cardiomyocytes fibrosis and apoptosis via the mitochondrial-mediated apoptotic pathway resulting from mitochondrial dysfunction.