A Bibliometric Review of Research Trends and Therapeutic Potential Reveals Natural Products as Major Regulators of Mitophagy in Kidney Disease.
TL;DR
This bibliometric analysis systematically reviews global research progress on mitophagy in kidney disease, with particular emphasis on the role of natural products as mitophagy modulators, and confirms that natural products represent a rich resource for mitophagy modulation in kidney disease.
Abstract
Objectives
Kidney disease constitutes a global health burden. Mitophagy, as a critical quality control mechanism, has emerged as an important therapeutic target. This bibliometric analysis systematically reviews global research progress on mitophagy in kidney disease, with particular emphasis on the role of natural products as mitophagy modulators.
Methods
Publications were retrieved from the Web of Science Core Collection. Bibliometric and visualization analyses were performed using Bibliometrix, CiteSpace, and VOSviewer software to assess publication trends, major contributors, collaborative networks, and research hotspots.
Results
Analysis of 472 articles identified China and the USA as dominant contributors. Keyword analysis identified "oxidative stress" and "apoptosis" as core themes. Among the reported pharmacological modulators, natural products and their derivatives occupy a predominant position. Representative agents identified include the natural compounds kaempferol, quercetin, esculetin, and dendrobine; the derivatives mitoTEMPO, MitoQ, and CoQ10; and traditional Chinese medicine formulas such as the Baoshentongluo Formula and Huangkui Capsule. These agents primarily regulate mitophagy via the PTEN-Induced Kinase 1 (PINK1)/Parkin pathway, the BCL2 Interacting Protein 3 (BNIP3)/BNIP3-like protein X (NIX) receptor pathway, and the FUN14 Domain-Containing 1 (FUNDC1) receptor pathway, alleviating renal injury by mitigating oxidative stress and inflammation.
Discussion
This field is undergoing a transition from basic mechanistic exploration toward therapeutic translation. Natural products are a major source of identified mitophagy regulators; however, challenges remain in the elucidation of active constituents, structural optimization, and preclinical validation. Future research should prioritize addressing these areas to accelerate the progression toward clinical application.
Conclusion
This study confirms that natural products represent a rich resource for mitophagy modulation in kidney disease. Advancing structure-activity relationship studies and rigorous preclinical evaluation of these compounds will be essential to develop novel therapeutic strategies.