Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions

At present, diabetes mellitus (DM) has been one of the most endangering healthy diseases. Current therapies contain controlling high blood sugar, reducing risk factors like obesity, hypertension, and so on; however, DM patients inevitably and eventually progress into different types of diabetes complications, resulting in poor quality of life. Unfortunately, the clear etiology and pathogenesis of diabetes complications have not been elucidated owing to intricate whole-body systems. The immune system was responsible to regulate homeostasis by triggering or resolving inflammatory response, indicating it may be necessary to diabetes complications. In fact, previous studies have been shown inflammation plays multifunctional roles in the pathogenesis of diabetes complications and is attracting attention to be the meaningful therapeutic strategy. To this end, this review systematically concluded the current studies over the relationships of susceptible diabetes complications (e.g., diabetic cardiomyopathy, diabetic retinopathy, diabetic peripheral neuropathy, and diabetic nephropathy) and inflammation, ranging from immune cell response, cytokines interaction to pathomechanism of organ injury. Besides, we also summarized various therapeutic strategies to improve diabetes complications by target inflammation from special remedies to conventional lifestyle changes. This review will offer a panoramic insight into the mechanisms of diabetes complications from an inflammatory perspective and also discuss contemporary clinical interventions. Inflammatory response and its related signaling pathways in diabetes complications. In the pathogenesis of diabetes complications, inflammatory factors, inflammasomes, immune cells, adhesion molecules, chemokine, and chemokine receptor are involved in the progression of diabetes complications through a series of inflammatory reactions. Related signaling pathways, including NF-kappa B, Toll-like receptors, MAPK, JAK/STAT, PI3K/Akt, mediate a series of inflammatory responses of diabetes complications. # image