Mitochondrial Dysfunction in Autoimmune Disorders
Mitochondria, the energy-producing organelles of eukaryotic cells, are involved in a myriad of cellular functions beyond ATP production, including calcium homeostasis, reactive oxygen species (ROS) generation, apoptosis regulation, and the modulation of immune responses. In autoimmune diseases, mitochondrial dysfunction is increasingly recognized as a key factor in disease pathogenesis. These disorders, characterized by the immune system's aberrant recognition and attack on self-antigens, often manifest in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS). This article delves into the mechanisms linking mitochondrial dysfunction to autoimmune disorders, highlighting cellular changes, signaling pathways, and potential therapeutic approaches.