Non-apoptotic programmed cell deaths in diabetic pulmonary dysfunction: the new side of advanced glycation end products

• Published in: Frontiers in endocrinology (Lausanne) Vol. 14; p. 1126661
• Main Authors: Dai, Yimin, Zhou, Shuang, Qiao, Lin, Peng, Zhao, Zhao, Jiuliang, Xu, Dong, Wu, Chanyuan, Li, Mengtao, Zeng, Xiaofeng, Wang, Qian
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 26.10.2023
• Subjects: advanced glycosylation end products; Apoptosis; Autophagic Cell Death; Diabetes Mellitus; diabetic pulmonary dysfunction; Endocrinology; Glycation End Products, Advanced - metabolism; Humans; inflammation; non-apoptotic programmed cell deaths; oxidative stress; Receptor for Advanced Glycation End Products - metabolism; advanced glycosylation end products; inflammation; non-apoptotic programmed cell deaths; diabetic pulmonary dysfunction; oxidative stress
• ISSN: 1664-2392; 1664-2392
• DOI: 10.3389/fendo.2023.1126661

Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mechanisms such as the production and accumulation of advanced glycation end products (AGEs), angiopathy, tissue glycation, oxidative stress, and systemic inflammation, recent studies have focused on programmed cell deaths (PCDs), especially the non-apoptotic ones, in diabetic pulmonary dysfunction. Non-apoptotic PCDs (NAPCDs) including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death have been found to have certain correlations with diabetes and relevant complications. The AGE–AGE receptor (RAGE) axis not only plays an important role in the traditional pathogenesis of diabetes lung disease but also plays an important role in non-apoptotic cell death. In this review, we summarize novel studies about the roles of non-apoptotic PCDs in diabetic pulmonary dysfunction and focus on their interactions with the AGE–RAGE axis.