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

Area of Science:

• Pulmonary Medicine
• Endocrinology
• Cell Biology

Background:

• Diabetes mellitus (DM) is a chronic metabolic disorder impacting multiple organ systems, including the lungs.
• Pulmonary dysfunction is a known complication of DM, but its mechanisms remain incompletely understood.
• Traditional mechanisms include advanced glycation end products (AGEs), angiopathy, oxidative stress, and inflammation.

Purpose of the Study:

• To review novel studies on the role of programmed cell deaths (PCDs) in diabetic pulmonary dysfunction.
• To highlight the significance of non-apoptotic PCDs (NAPCDs) in the context of diabetes-related lung complications.
• To examine the interplay between NAPCDs and the AGE-RAGE axis in diabetic lung disease pathogenesis.

Main Methods:

• Literature review of recent studies on diabetic pulmonary dysfunction.
• Focus on programmed cell death pathways, particularly non-apoptotic forms.
• Analysis of the AGE-RAGE axis involvement in diabetic lung pathology and cell death.

Main Results:

• Non-apoptotic PCDs (NAPCDs), including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death, are correlated with diabetes and its complications.
• The AGE-RAGE axis is implicated in both traditional diabetic lung disease mechanisms and NAPCDs.
• Emerging evidence points to NAPCDs as critical contributors to pulmonary dysfunction in diabetes.

Conclusions:

• Non-apoptotic PCDs represent a significant, yet understudied, area in diabetic pulmonary dysfunction.
• The AGE-RAGE axis is a central player, linking traditional pathways with novel cell death mechanisms.
• Further research into NAPCDs and the AGE-RAGE axis may reveal new therapeutic targets for diabetic lung disease.