**Background of ATP Antibodies**
ATP antibodies, primarily targeting ATP synthase (complex V) or related enzymes, are linked to autoimmune and metabolic disorders. ATP synthase, a mitochondrial enzyme crucial for oxidative phosphorylation, generates cellular energy (ATP). Autoantibodies against its subunits (e.g., α/β subunits) are implicated in conditions like autoimmune hepatitis, systemic lupus erythematosus (SLE), and anti-phospholipid syndrome (APS). These antibodies may disrupt mitochondrial function, impairing energy production and promoting tissue damage.
First identified in autoimmune hepatitis patients, anti-ATP synthase antibodies are detected via ELISA or immunoblotting. Their presence often correlates with disease severity, suggesting a role in pathogenesis. In APS, antibodies targeting β-subunits may bind endothelial cells, triggering thrombosis. Research also explores their involvement in neurodegenerative diseases, where mitochondrial dysfunction is pivotal.
While mechanisms remain unclear, molecular mimicry between microbial and human ATP synthase components is hypothesized to initiate autoimmunity. Current studies focus on therapeutic strategies to neutralize these antibodies or modulate mitochondrial resilience. Understanding ATP antibodies enhances insights into autoimmune pathophysiology and informs diagnostic or therapeutic innovations.