Abstract

Anaemia is a common and underappreciated complication of diabetes that worsens quality of life, increases 
cardiovascular risk, and accelerates progression of diabetic complications. Multiple interacting mechanisms 
contribute to diabetes-associated anaemia, including reduced erythropoietin (EPO) production, iron dysregulation, 
shortened red blood cell (RBC) lifespan, bone marrow suppression, and chronic inflammation. Oxidative stress
driven by hyperglycaemia, dyslipidaemia, mitochondrial dysfunction, and advanced glycation end-products-is a 
central, unifying mediator that perturbs erythropoiesis at molecular and cellular levels. Beyond direct oxidative 
damage to erythroid precursors and mature RBCs, redox imbalance alters signaling pathways (HIF, JAK/STAT, 
NF-κB), disrupts iron handling (hepcidin–ferroportin axis), and modulates neuro-immune interactions that can 
influence hematopoiesis. Neuromodulators (endogenous and drug-like agents that alter neural input to 
hematopoietic and immune compartments) and natural product antioxidants (polyphenols, flavonoids, terpenoids, 
alkaloids, and omega-3 fatty acids) are emerging as promising adjuncts for correcting redox-driven defects in 
diabetic erythropoiesis. This review integrates mechanistic insights into oxidative stress–mediated suppression of 
erythropoiesis in diabetes, evaluates evidence that neuromodulatory pathways intersect with hematopoietic 
regulation, and examines preclinical and clinical data for natural antioxidants as supportive therapies in diabetic 
anaemia. We highlight therapeutic strategies, formulation and safety considerations, and research priorities needed 
to translate these biologically plausible interventions into clinical practice.