Background: Systemic Lupus Erythematosus (SLE) is a polysystem autoimmune
disease that adversely affects human health. Various organs can be affected, including the
kidney or brain. Traditional treatment methods for SLE primarily rely on glucocorticoids and
immunosuppressors. Unfortunately, these therapeutic agents cannot prevent a high recurrence
rate after SLE remission. Therefore, novel therapeutic targets are urgently required.
Methods: A systematic search of the published literature regarding the abnormal structure and
function of mitochondria in SLE and therapies targeting mitochondria was performed in several
Results: Accumulating evidence indicates that mitochondrial dysfunction plays important
roles in the pathogenesis of SLE, including influencing mitochondrial DNA damage, mitochondrial
dynamics change, abnormal mitochondrial biogenesis and energy metabolism, mitophagy,
oxidative stress, inflammatory reactions, apoptosis and NETosis. Further investigation
of mitochondrial pathophysiological roles will result in further clarification of SLE. Specific
lupus-induced organ damage also exhibits characteristic mitochondrial changes.
Conclusion: This review aimed to summarize the current research on the role of mitochondrial
dysfunction in SLE, which will necessarily provide potential novel therapeutic targets