Review
Version 1
Preserved in Portico This version is not peer-reviewed
Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy
Version 1
: Received: 31 May 2024 / Approved: 3 June 2024 / Online: 3 June 2024 (07:22:31 CEST)
A peer-reviewed article of this Preprint also exists.
Wątroba, M.; Grabowska, A.D.; Szukiewicz, D. Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy. Int. J. Mol. Sci. 2024, 25, 7527. Wątroba, M.; Grabowska, A.D.; Szukiewicz, D. Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy. Int. J. Mol. Sci. 2024, 25, 7527.
Abstract
Diabetes mellitus (DM) is the most common metabolic disease in humans, and its prevalence is increasing worldwide in parallel with the obesity pandemic. A lack of insulin or insulin resistance, and consequently hyperglycemia, leads to many systemic disorders, among which diabetic encephalopathy (DE) is a long-term complication of the central nervous system (CNS), characterized by cognitive impairment and motor dysfunctions. The role of oxidative stress and neuroinflammation in the pathomechanism of DE has been proven. Fractalkine (CX3CL1) has unique properties as an adhesion molecule and chemoattractant, and by acting on its only receptor, CX3CR1, it regulates the activity of microglia in physiological states and neuroinflammation. Depending on the clinical context, CX3CL1-CX3CR1 signaling may have neuroprotective effects by inhibiting the inflammatory process in microglia or, conversely, maintaining/intensifying inflammation and neurotoxicity. This review discusses the evidence supporting that the CX3CL1-CX3CR1 pair is neuroprotective and other evidence that it is neurotoxic. Interrupting the vicious cycle within neuron-microglia interactions may be a therapeutic goal in DE by limiting the inflammatory response.
Keywords
diabetic encephalopathy; chemokine CX3CL1; fractalkine; central nervous system; neuroinflammation; diabetes mellitus; hyperglycemia; advanced glycation end products; CX3CL1/CX3CR1 axis
Subject
Medicine and Pharmacology, Pathology and Pathobiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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