Thioredoxin (TXN) is a multifunctional redox protein that serves as a metabolic regulator of cellular oxidative balance. Mechanistically, TXN functions as a protein-disulfide reductase that maintains cellular redox homeostasis and detoxifies hydrogen peroxide 1, working alongside thioredoxin reductase (TXNRD) to reduce oxidative stress and prevent ROS accumulation 2. TXN expression is particularly elevated in regulatory B cells, where it maintains mitochondrial membrane potential and physiological ROS levels essential for cell differentiation and function 3. Disruption of TXN activity or expression impairs redox balance and contributes to multiple pathological conditions. Reduced TXN activity increases intracellular ROS, disrupts GSH/ROS balance, and can trigger oxidative cell death 4. TXN dysfunction is implicated in systemic lupus erythematosus (SLE), where Breg cell deficiency correlates with elevated ROS and decreased Trx+ B cells; exogenous thioredoxin restores Breg function in SLE patients 3. TXN emerges as a diagnostic biomarker for severe asthma 5 and sepsis 6, where it correlates with immune cell infiltration and oxidative stress status. Clinically, TXN represents a therapeutic target for cancer therapy through TXNRD1 inhibition, which increases oxidative stress in cancer cells 2, and is associated with nonhealing diabetic foot ulcers 7.