Mitochondrial autophagy in diabetes-related cognitive decline and skin ulcers: Mechanistic insights and therapeutic implications

Figure 2 Autoimmune destruction of pancreatic β cells in type 1 diabetes. The diagram illustrates the pathophysiology of type 1 diabetes mellitus, showing the progressive autoimmune attack on insulin-producing β cells within the pancreatic islets of Langerhans (left panel). The normal pancreatic islet architecture contains α cells (producing glucagon), β cells (producing insulin), and δ cells (producing somatostatin) (middle panel). In type 1 diabetes, autoreactive cytotoxic T cells recognize β cell-specific antigens and mount an immune attack against insulin-producing cells, whereas α and δ cells remain largely unaffected (right panel). The end result of this autoimmune process is the selective destruction of β cells, leading to complete insulin deficiency, whereas glucagon and somatostatin production from α and δ cells continues. This autoimmune-mediated β-cell destruction results in the characteristic hyperglycemia and insulin dependence observed in type 1 diabetes patients. This figure was created by BioRender.com (Supplementary material).