이명식 (순천향대학교)

한빛사논문

조회247

순천향대학교

CV File 458 kb

Trends Endocrinol. Metab., Jul 24 2024, S1043-2760(24)00170-X | https://doi.org/10.1016/j.tem.2024.06.010 Autophagy and lysosomal dysfunction in diabetes and its complications

Catherine Arden ¹, Seo H. Park ², Xaviera Riani Yasasilka ², Eun Y. Lee³, Myung-Shik Lee ^2,4

¹Biosciences Institute, Newcastle University, Newcastle Upon Tyne, UK

²Soonchunhyang Institute of Medi-bio Science, Soonchunhyang University, Cheonan, Republic of Korea

³Division of Nephrology, Department of Internal Medicine, Soonchunhyang University College of Medicine, Cheonan, Republic of Korea

⁴Division of Endocrinology, Department of Internal Medicine and Department of Microbiology and Immunology, Soonchunhyang University College of Medicine, Cheonan, Republic of Korea

Correspondence: Myung-Shik Lee

Abstract

Autophagy is critical for energy homeostasis and the function of organelles such as endoplasmic reticulum (ER) and mitochondria. Dysregulated autophagy due to aging, environmental factors, or genetic predisposition can be an underlying cause of not only diabetes through β-cell dysfunction and metabolic inflammation, but also diabetic complications such as diabetic kidney diseases (DKDs). Dysfunction of lysosomes, effector organelles of autophagic degradation, due to metabolic stress or nutrients/metabolites accumulating in metabolic diseases is also emerging as a cause or aggravating element in diabetes and its complications. Here, we discuss the etiological role of dysregulated autophagy and lysosomal dysfunction in diabetes and a potential role of autophagy or lysosomal modulation as a new avenue for treatment of diabetes and its complications.

논문정보

형식Review Paper
게재일2024년 07월 (BRIC 등록일 2024-07-29)
연구진국내(교신)+국외 연구진
분야 의약학 > 면역의학

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