Molecular and biochemical mechanisms of diabetic encephalopathy

Igor Belenichev; Olena Aliyeva; Olena Popazova; Nina Bukhtiyarova

doi:10.18388/abp.2020_6953

Igor Belenichev Department of Pharmacology and Medical Formulation with Course of Normal Physiology, Zaporizhzhia State Medical and Pharmaceutical University, Zaporizhzhia, Ukraine
Olena Aliyeva Department of Medical Biology, Parasitology and Genetics, Zaporizhzhia State Medical and Pharmaceutical University, Zaporizhzhia, Ukraine https://orcid.org/0000-0003-1287-674X
Olena Popazova Department of Histology, Cytology and Embryology, Zaporizhzhia State Medical and Pharmaceutical University, Zaporizhzhia, Ukraine
Nina Bukhtiyarova Department of Clinical Laboratory Diagnostics, Zaporizhzhia State Medical and Pharmaceutical University, Zaporizhzhia, Ukraine

DOI: https://doi.org/10.18388/abp.2020_6953

Abstract

Diabetes mellitus is one of the important independent risk factors for the development of neurological disorders such as ischemic stroke, transient ischemic attacks, vascular dementia and neurodegenerative processes. Hyperglycemia plays a crucial role as a trigger in the pathogenesis of these disorders. In this review, we summarize the existing data on the molecular mechanisms of diabetic encephalopathy development, consider the features of oxidative and nitrosative stresses, changes in the thiol-disulfide system, as well as mitochondrial and endothelial dysfunction in diabetes. We focus on the role of HSP 70 in cellular responses in diabetic encephalopathy. HSP70 protein is an important component of the endogenous system of neuroprotection. It acts as an intracellular chaperone, providing the folding, retention, and transport of synthesized proteins, as well as their degradation under both normoxic and stress-induced denaturation conditions. HSP70 can be considered a molecular marker and a promising therapeutic target in the treatment of diabetes mellitus.