Mitochondrial Dysfunction and Hematopoietic Impairment in Diabetes: The Oxidative Stress Connection

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, which leads to systemic complications. Among these, mitochondrial dysfunction plays a critical role in hematopoietic impairment, primarily through the induction of oxidative stress. The mitochondrial electron transport chain (ETC) is a significant source of reactive oxygen species (ROS) in diabetes, leading to oxidative damage in hematopoietic stem and progenitor cells (HSPCs). This review explores the intricate relationship between mitochondrial dysfunction, oxidative stress, and hematopoietic abnormalities in diabetes, discussing underlying molecular mechanisms and potential therapeutic strategies. We highlight the impact of excessive ROS production on hematopoietic homeostasis, including impaired erythropoiesis, leukopenia, and thrombocytopenia, which contribute to anemia, immune dysfunction, and increased risk of cardiovascular complications. Furthermore, we examine emerging therapeutic approaches aimed at mitigating oxidative stress and restoring mitochondrial function to improve hematopoietic health in diabetic patients. Keywords: Mitochondrial dysfunction, Hematopoiesis, Diabetes, Oxidative stress, Reactive oxygen species, Hematopoietic stem cells, Antioxidant therapy