Complications of type 1 diabetes: new molecular findings.
Interventions targeting the treatment of diabetic complications have not been nearly as successful as initially estimated, despite a marked improvement in therapeutic options for diabetes. The need for understanding why some very promising interventions have failed demands a closer look at the pathomechanisms of the complications. Great strides have been made in understanding the pathology, and several important hypotheses have emerged in recent years. On this basis, Brownlee and coworkers suggested a unifying hypothesis integrating various mechanisms discussed in past years with an overproduction of reactive oxygen species as an initiating cause. This hypothesis and further hypotheses, as well as mechanisms, are highlighted in this article. The field of pathomechanisms of diabetic complications is very wide, and any attempt to completely cover it within a single article is unrealistic. Therefore, our purpose is to present the most relevant concepts underlying diabetic complications in an attempt to contribute to a better understanding and pinpoint areas that warrant further research.
Stirban
Alin
A
Diabetes Clinic, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany. astirban@hdz-nrw.de
Rösen
Peter
P
Tschoepe
Diethelm
D
D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000235:genetics* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000209:etiology; D003929:Diabetic Neuropathies / Q000209:etiology; D003930:Diabetic Retinopathy / Q000209:etiology; D005609:Free Radicals; D006595:Hexosamines; D006801:Humans; D008928:Mitochondria; D017382:Reactive Oxygen Species
D005609:Free Radicals; D006595:Hexosamines; D017382:Reactive Oxygen Species