Year: 2025
Type: article
Abstract: Neuroinflammation is a key pathological component in neurodegenerative diseases, particularly in Parkinson’s disease (PD). The transcription factor HIF-1α plays a central role in regulating neuroinflammatory processes by integrating metabolic and immune responses under conditions of hypoxia and inflammation. Microglia, the main effector of neuroinflammation, undergo phenotypic and functional changes mediated by HIF-1α. HIF-1α modulates the activity of pro-inflammatory (IL-1β, IL-6, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokines, regulates metabolic pathways such as aerobic glycolysis via the AKT-mTOR axis, and influences Th17/Treg cell differentiation.In addition, HIF-1α interacts with signaling pathways including NF-κB, JAK-STAT, and Notch, making it a critical factor in the progression of neurodegeneration. Pharmacological modulation of HIF-1α (e.g., with FG-4592 or YC-1 inhibitors) shows promise for the treatment of neuroin-flammatory conditions.Thus, HIF-1α functions as an integrative regulator of neuroinflam-mation, positioning it as a promising therapeutic target for PD and other neurodegenerative disorders. Key words: epigenetics, cardiometabolic diseases, diabetes, obesity, gene expression, DNA methylation
Authors: Illya Farkhidinov, Zoya Serebrovska
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4412418878