Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy DOI Open Access
Mateusz Wątroba,

Anna D. Grabowska,

Dariusz Szukiewicz

et al.

Published: June 3, 2024

Diabetes mellitus (DM) is the most common metabolic disease in humans, and its prevalence increasing worldwide parallel with obesity pandemic. A lack of insulin or resistance, consequently hyperglycemia, leads to many systemic disorders, among which diabetic encephalopathy (DE) a long-term complication central nervous system (CNS), characterized by cognitive impairment motor dysfunctions. The role oxidative stress neuroinflammation pathomechanism DE has been proven. Fractalkine (CX3CL1) unique properties as an adhesion molecule chemoattractant, acting on only receptor, CX3CR1, it regulates activity microglia physiological states neuroinflammation. Depending clinical context, CX3CL1-CX3CR1 signaling may have neuroprotective effects inhibiting inflammatory process or, conversely, maintaining/intensifying inflammation neurotoxicity. This review discusses evidence supporting that pair other neurotoxic. Interrupting vicious cycle within neuron-microglia interactions be therapeutic goal limiting response.

Language: Английский

Chemokine CX3CL1 (Fractalkine) Signaling and Diabetic Encephalopathy DOI Open Access
Mateusz Wątroba,

Anna D. Grabowska,

Dariusz Szukiewicz

et al.

Published: June 3, 2024

Diabetes mellitus (DM) is the most common metabolic disease in humans, and its prevalence increasing worldwide parallel with obesity pandemic. A lack of insulin or resistance, consequently hyperglycemia, leads to many systemic disorders, among which diabetic encephalopathy (DE) a long-term complication central nervous system (CNS), characterized by cognitive impairment motor dysfunctions. The role oxidative stress neuroinflammation pathomechanism DE has been proven. Fractalkine (CX3CL1) unique properties as an adhesion molecule chemoattractant, acting on only receptor, CX3CR1, it regulates activity microglia physiological states neuroinflammation. Depending clinical context, CX3CL1-CX3CR1 signaling may have neuroprotective effects inhibiting inflammatory process or, conversely, maintaining/intensifying inflammation neurotoxicity. This review discusses evidence supporting that pair other neurotoxic. Interrupting vicious cycle within neuron-microglia interactions be therapeutic goal limiting response.

Language: Английский

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