<p>Parkinson’s disease (PD) is a common neurodegenerative disease with multiple causes and complex mechanisms. Mitochondrial dysfunction is the main cause and central event of dopaminergic neuron degeneration in PD. Therefore, studying mitochondrial dysfunction plays an important role in understanding the pathogenesis of PD. In the future, mitochondrial dysfunction becomes an important therapeutic target for this disease. This article focuses on the mitochondrial molecular mechanism of neurodegeneration, including reactive oxygen species generation, mitochondrial autophagy, and mitochondrial dynamics, etc., and the potential targets for PD therapy. This article also discusses other potential treatment strategies, such as mitochondrial transplantation, targeted microRNA, use of stem cells and exercise, these may provide valuable insights for clinical practice. A better understanding of the role of mitochondria in the pathophysiology of PD may provide fundamental principles for designing new therapeutic interventions to combat PD.</p>