Publication date: Jun 25, 2025
The pathological mechanism of Parkinson’s disease (PD) is complex and affected by multi-system and multi-level factors including mitochondrial dysfunction (MD). It has been demonstrated that all patients with PD have a marked loss of dopaminergic neurons in the substantial nigra pars compacta, and MD is an important initial factor causing dopaminergic neuron degeneration. Clinical practice has shown that acupuncture has a positive role in the treatment of PD. In the present article, we summed up recent research results about the mechanisms of acupuncture underlying improvement of PD from the standpoint of mitochondrial function. Acupuncture has been shown to be able in improving mitochondrial function, and restoring mitochondrial homeostasis, and protecting the normal morphological structure of mitochondria. It can also regulate the expression of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1α), adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK), and Sirtuins (SIRT) to take part in mitochondrial biogenesis; decrease the levels of dynamin-related protein 1 (Drp1), mitochondrial fission factor (MFF), and mitochondrial fission protein 1 (Fis1) protein to preserve mitochondrial dynamic stability; and modulate the expression of PTEN-induced putative kinase 1 (PINK1), Parkin, P62, microtubule-associated protein light chain 3Ⅱ (LC3Ⅱ), and Beclin1 to promote autophagy. In addition, through controlling mitochondrial energy metabolism, preserving calcium homeostasis, reducing oxidative stress, and preventing neuronal apoptosis, acupuncture can also help improve mitochondrial dysfunction and prevent the onset and progression of PD. However, more researches are warranted to fully unravel the underlying mechanisms of acupuncture intervention before it can be popularized in clinical settings.
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | Parkinson’s disease |
| disease | MESH | mitochondrial dysfunction |
| disease | MESH | neuron degeneration |
| pathway | KEGG | Peroxisome |
| drug | DRUGBANK | Adenosine phosphate |
| pathway | REACTOME | Mitochondrial biogenesis |
| drug | DRUGBANK | Trihexyphenidyl |
| drug | DRUGBANK | Profenamine |
| pathway | REACTOME | Autophagy |
| pathway | REACTOME | Metabolism |
| drug | DRUGBANK | Calcium |
| disease | MESH | oxidative stress |
| pathway | REACTOME | Apoptosis |
| pathway | KEGG | Parkinson disease |