About this Research Topic
Cardiovascular events, nephropathy, retinopathy, and diabetic neuropathies represent the “classical” and most studied diabetic related long-term complications. The endothelium appears to be the common substrate hit by hyperglycaemia, insulin resistance, and other cardiovascular risk factors. The discovery of novel disease pathways in this regard is contributing to the identification of potential therapeutic targets which offer thrilling opportunities for tackling vascular complications of diabetes. In addition, recent randomized controlled trials have already shown significant reductions in the risk of cardiovascular and renal outcomes associated with the use of novel anti-diabetes drugs, such as SGLT2i and GLP1-RA, promising a radical change in the panorama of vascular disease in diabetes in the near future.
However, the systemic effects of diabetes are extensive, and upcoming complications of diabetes have been recently evaluated since strong epidemiological association between diabetes and other high-prevalence disorders have been found, suggesting the existence of complex physiopathology.
In this respect, there is emerging evidence that bone is a target organ of diabetes: an increased risk of bone fragility and osteoporotic fractures in both type 1 (T1D) and type 2 (T2D) diabetes compared to the general population has been shown. Moreover, since bone mineral density (BMD) is generally increased in T2D compared with controls, there are some lines of evidences that specific alterations in bone quality may increase fracture risk in diabetic subjects irrespective of BMD. Multiple pathways have been considered to contribute to diabetic osteopathy, including hyperglycaemia and accumulation of advanced glycation end-products in bone collagen, defects in insulin secretion or activity, inadequate vitamin D status, osteocalcin dysmetabolism, and increased proinflammatory cytokines and adipokine levels.
Furthermore, strong interaction between diabetes, bone, and vascular impairment has been recently recognized, leading to the identification of a bone-vascular axis which may be a novel target to tackle cardiovascular complications of diabetes. Thus, vascular calcification plays a key role in the pathogenesis of diabetic macrovascular disease and novel biomarkers of vascular function and is potentially involved in the crosstalk between bone and vascular disease. It should be further investigated in order to establish new strategies toward prevention or early diagnosis of bone-vascular axis disfunctions.
Another outstanding issue concerns the link between diabetes, vascular dysfunction, and dementia. Indeed, thanks to the increasing interests in aging-related diseases, diabetes-related cognitive impairment is attracting great attention. To date, there is convincing epidemiological evidence showing an increased risk of developing Alzheimer’s disease (AD) and other neurodegenerative disorders in diabetic subjects, supporting the existence of multiple pathogenic cascades induced by impaired cerebral glucose metabolism that could result in neuronal degeneration and consequently cognitive deficits in diabetic patients. Among these pathogenic processes, insulin signalling and imbalance in glucagon/insulin homeostasis are highly emphasized and characterized as major pathogenic mechanisms, contributing to the formation of amyloid deposits in the brain and AD. Similarly, a potential role of altered thiamine metabolism has been recently discussed.
This Research Topic aims to further our understanding of the system-wide expression of diabetes, evaluating the “novel” complications of the disease, describing the common pathogenetic pathways involved in the interplay between diabetes and organ damage, and summarizing the most recent advances in the understanding and treatment of classical vascular complications. We welcome review, mini review, and original research articles.
However, the systemic effects of diabetes are extensive, and upcoming complications of diabetes have been recently evaluated since strong epidemiological association between diabetes and other high-prevalence disorders have been found, suggesting the existence of complex physiopathology.
In this respect, there is emerging evidence that bone is a target organ of diabetes: an increased risk of bone fragility and osteoporotic fractures in both type 1 (T1D) and type 2 (T2D) diabetes compared to the general population has been shown. Moreover, since bone mineral density (BMD) is generally increased in T2D compared with controls, there are some lines of evidences that specific alterations in bone quality may increase fracture risk in diabetic subjects irrespective of BMD. Multiple pathways have been considered to contribute to diabetic osteopathy, including hyperglycaemia and accumulation of advanced glycation end-products in bone collagen, defects in insulin secretion or activity, inadequate vitamin D status, osteocalcin dysmetabolism, and increased proinflammatory cytokines and adipokine levels.
Furthermore, strong interaction between diabetes, bone, and vascular impairment has been recently recognized, leading to the identification of a bone-vascular axis which may be a novel target to tackle cardiovascular complications of diabetes. Thus, vascular calcification plays a key role in the pathogenesis of diabetic macrovascular disease and novel biomarkers of vascular function and is potentially involved in the crosstalk between bone and vascular disease. It should be further investigated in order to establish new strategies toward prevention or early diagnosis of bone-vascular axis disfunctions.
Another outstanding issue concerns the link between diabetes, vascular dysfunction, and dementia. Indeed, thanks to the increasing interests in aging-related diseases, diabetes-related cognitive impairment is attracting great attention. To date, there is convincing epidemiological evidence showing an increased risk of developing Alzheimer’s disease (AD) and other neurodegenerative disorders in diabetic subjects, supporting the existence of multiple pathogenic cascades induced by impaired cerebral glucose metabolism that could result in neuronal degeneration and consequently cognitive deficits in diabetic patients. Among these pathogenic processes, insulin signalling and imbalance in glucagon/insulin homeostasis are highly emphasized and characterized as major pathogenic mechanisms, contributing to the formation of amyloid deposits in the brain and AD. Similarly, a potential role of altered thiamine metabolism has been recently discussed.
This Research Topic aims to further our understanding of the system-wide expression of diabetes, evaluating the “novel” complications of the disease, describing the common pathogenetic pathways involved in the interplay between diabetes and organ damage, and summarizing the most recent advances in the understanding and treatment of classical vascular complications. We welcome review, mini review, and original research articles.
Keywords: Diabetic Complications
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
