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

Abstract

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.

Extrapulmonary Comorbidities Associated with Chronic Obstructive Pulmonary Disease: A Review

“… 43 In addition, the advanced glycation end products (AGEs) associated with hyper glycaemia can trigger inflammation and attenuate alveolar retraction, thus exacerbating the patient’s ventilatory deficits. 44 At the same time, diabetic autonomic neuropathy can also dysregulate airway diastolic function. 45 Additionally, hypoxia has the potential to impact glucose metabolism and insulin sensitivity, 29 leading to an increased risk of excessive oxidation and oxidative stress.…”