The development and emerging trends in Parkinson's disease from the perspective of mitochondrial dysfunction: a bibliometric analysis using CiteSpace.

BACKGROUND

Parkinson's disease (PD) is an increasingly prevalent neurodegenerative disease. Although diagnosis and management have improved, the global burden remains a significant concern. Currently, it is challenging to achieve effective treatment due to the gap in understanding the pathological cascade mechanism of PD. Converging clinical, genetic, and experimental evidence suggests that mitochondrial dysfunction plays a central role in the pathogenesis of PD. Therefore, research progress and the systematic exploration of the remaining unknowns regarding mitochondrial dysfunction in PD are clarifying pathogenesis and guiding therapeutic strategies.

METHODS

Using CiteSpace, we collected 5,040 publications on PD and mitochondrial dysfunction from Web of Science Core Collection. Visualization analysis based on betweenness centrality, count, and burst values aims to identify current research hotspots and predict emerging trends.

RESULTS

Recent years have seen a significant increase in publications on PD and mitochondrial dysfunction. Current research hotspots focus on "oxidative stress," "alpha-synuclein," "rotenone," "PINK1/Parkin pathway," "complex I," and various neurodegenerative diseases. Analysis predicts "NLRP3 inflammasome," "cognitive impairment," "gut microbiota," and "insulin resistance" as potential future research frontiers. Multidimensional pathway exploration is crucial for comprehensively understanding PD pathogenesis, with mitochondrial dysfunction serving as a central hub that represents a key future therapeutic target.

CONCLUSION

The multipathology of PD creates synergistic therapeutic opportunities, particularly through mitochondria-focused approaches that modulate core disease mechanisms. On this basis, enhancing mitochondrial biogenesis is a fundamental path forward, moving beyond protection to actively restore mitochondrial networks and promote neuronal recovery. These findings help comprehend PD's complex pathogenesis and guide precision therapeutic strategies.