Autophagy and lysosomal dysfunction in diabetes and its complications.
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.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
The paper discusses the role of autophagy and lysosomal dysfunction in diabetes and its complications, which are indeed related to aging and metabolic health. However, it primarily focuses on the mechanisms of disease rather than addressing the root causes of aging or proposing significant interventions for lifespan extension. The findings contribute to understanding diabetes in the context of aging but do not present groundbreaking insights that would significantly advance the field of longevity research. Thus, while relevant, its impact is limited.
Author of this paper? Send a correction.