Abstract
AbstractThe objective of this manuscript is to provide a comprehensive understanding of the general etiology of diabetic ulcers. While it is commonly perceived that “peripheral neuropathy” is the sole cause of diabetic ulcers due to reduced arterial blood supply and impaired venous circulation to the wound, there is a significant oversight at the nano-molecular level regarding the impact of high blood glucose/glycans in diabetic patients. A significant number of research literature talk about the influence of high blood glucose, the impact of glycosylation, the role of lysyl oxidase in collagen maturation along with the impact on peripheral nerve cells causing neuropathy. Such peripheral neuropathy could also be playing a major role in the reduction of arterial blood supply. Through this review article, the author aims to shed light on the unexplored mechanisms involving the glycosylation of lysine residues caused by excessive blood glucose/glycans/polysialic acids, and other related processes. These alterations disrupt the normal pathway of oxidative deamination of lysine residues, which are supposed to serve as substrates for lysyl oxidase. Consequently, the conversion of amino groups to aldehyde groups is impeded, leading to a disruption in the aldol-condensation reaction necessary for the regular maturation of wound bed collagen and proper healing of the wound.
Publisher
Springer Science and Business Media LLC
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