Dr.MasayukiKuroda Japan

Dr.MasayukiKuroda
Masayuki Kuroda, Ph.D., is a biomedical scientist specializing in gene therapy, cell engineering, and translational medicine. He earned his Ph.D. in Pharmaceutical Sciences from Okayama University in 1993, where he conducted research in microbiology and acquired foundational expertise in molecular and cellular biology. He subsequently trained at Harvard Medical School and Wayne State University School of Medicine, further strengthening his background in molecular biology and gene regulation. Upon returning to Japan, Dr. Kuroda joined Kochi Medical School (later reorganized as Kochi University), where his research shifted toward virology and the development of viral therapeutic vectors, marking the beginning of his long-standing involvement in gene therapy technologies. In addition to his work in virology, he contributed to education and broader microbiological research within the department. He later transitioned to CellGenTech, Inc. as a Manager, participating in the development of cell-based therapeutic platforms. Since 2007, Dr. Kuroda has been affiliated with Chiba University in the fields of clinical gene medicine and cellular therapeutics. He currently serves as an Associate Professor at the Center for Advanced Medicine, Chiba University Hospital. Dr. Kuroda’s current research focuses on engineering therapeutic cells—particularly ex vivo gene/cell therapy using adipocytes—to establish sustained in vivo delivery systems for bioactive molecules such as enzymes and metabolites. His work harnesses the unique biological features of adipocytes, including their long-term survival, metabolic stability, high secretory capacity, and favorable safety profile. By integrating adipocyte engineering with translational research, he aims to develop next-generation therapies for rare genetic diseases and metabolic disorders.

21 MARCH

Time Session
08:30
10:00
New Development in Dyslipidemia Management
  • Kathryn TanHong Kong, China Speaker Lipoprotein(a): What Endocrinologists Need to KnowLipoprotein(a) [Lp(a)] is a cholesterol-rich LDL-like particle with apolipoprotein(a) covalently linked to apolipoprotein B100 via a disulfide bond. Lp(a) is synthesized within the liver and there is a general inverse correlation between Lp(a) isoform size and plasma Lp(a) concentrations. About 90% of plasma Lp(a) concentration is genetically determined and plasma levels can modestly rise after menopause in women, and in conditions like hypothyroidism, nephrotic syndrome. It has been shown that elevated Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Although Lp(a) concentration does vary with ethnicity, relationships between Lp(a) concentration and ASCVD risk remain similar across different ethnic groups. Elevated Lp(a) is considered a cardiovascular risk-enhancing or amplification factor, and recent guidelines and consensus have increasingly recommended universal screening for Lp(a). There are as yet, no approved therapies for elevated Lp(a). Current management focuses on intensifying control of concurrent risk factors, particularly LDL-C, to reduce ASCVD risk. Amongst existing lipid-lowering drugs, only proprotein convertase subtilisin/kexin type 9 inhibitors can lower Lp(a) levels modestly. Emerging RNA-based and small-molecule therapeutics are under development and are showing promising Lp(a)-lowering effects up to 80-90%. Ongoing phase 3 cardiovascular outcomes trials will determine whether effectively lowering Lp(a) can translate to cardiovascular benefit.
  • Masayuki KurodaJapan Speaker Autologous Implantation of Genetically Modified Adipocytes Expressing LCAT for the Treatment of Familial LCAT Deficiency
  • Sung Hee ChoiKorea Speaker Novel and Future Lipid-Lowering Therapy
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