Evidence suggests that specific alterations in DNA methylation play a central role in ID pathogenesis, affecting key neurodevelopmental processes such as neuronal maturation, synaptogenesis, and memory formation
Zinc deficiency correlates with the severity of diabetic complications, including peripheral neuropathy
SCFA (acetate, propionate and butyrate) production also increased upon apigenin treatment (Reference Van Dorsten, Peters and Gross55) (Fig
Nano-HBOCs for wound healing O 2 plays a key role in wound healing [203] by promoting cell proliferation, accelerating angiogenesis, reducing infection, and increasing collagen synthesis [204, 205]
The mitochondrial impairment in FM is evident from reduced bioenergetic health index (BHI) and increased mitochondrial miRNAs (mitomiR-145-5p) in peripheral blood mononuclear cells (PBMCs), which regulate oxidative stress responses ( Observational studies indeed suggest that oxidative stress disrupts neurotransmitter regulation, particularly serotonin ( Lipid metabolism alterations and fibromyalgia Recent metabolomic studies have highlighted significant alterations in lipid metabolism in FM patients, particularly shifts in phospholipid composition ( Notably, LPC (16:0), a lipid oxidation product, is elevated in FM and directly activates acid-sensing ion channel 3 (ASIC3) on nociceptors, leading to hyperalgesia in animal models ( Antioxidant defense impairment in fibromyalgia The imbalance between ROS production and antioxidant defenses is a feature of FM pathophysiology ( Several studies have shown that antioxidant enzyme deficiencies, including low SOD, glutathione peroxidase, and catalase, correlate inversely with disease severity measures such as the Fibromyalgia Impact Questionnaire (FIQR), pain scores, and anxiety levels ( Further, the nuclear factor erythroid 2-related factor 2 (NRF2) pathway is a master regulator of antioxidant and cytoprotective gene expression, crucial for cellular defense against oxidative stress
