The potential therapeutic role of ginsenosides on fibrosis-associated diseases: a review on molecular mechanisms and call for further research.
10.1016/S1875-5364(25)60817-X
- Author:
Mengguang WEI
1
;
Yue ZHANG
1
;
Xiaomeng SUN
1
;
Lianwen QI
2
;
Qun LIU
3
,
4
Author Information
1. State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.
2. State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China; Clinical Metabolomics Center, China Pharmaceutical University, Nanjing 211198, China. Electronic address: Qilw@cpu.edu.cn.
3. State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China. Electronic address: liuquncpu@
4. com.
- Publication Type:Review
- Keywords:
Ginsenosides;
Liver fibrosis;
Mechanisms;
Myocardial fibrosis;
Pulmonary fibrosis;
Renal fibrosis
- MeSH:
Ginsenosides/pharmacology*;
Humans;
Fibrosis/drug therapy*;
Animals;
Panax/chemistry*;
Drugs, Chinese Herbal/therapeutic use*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2025;23(6):673-686
- CountryChina
- Language:English
-
Abstract:
Fibrosis is characterized as an aberrant reparative process involving the direct replacement of damaged or deceased cells with connective tissue, leading to progressive architectural remodeling across various tissues and organs. This condition imposes a substantial burden, resulting in considerable morbidity and mortality. Ginseng (Panax ginseng C. A. Meyer), renowned for its medicinal properties, has been incorporated as a key component in Chinese patent medicines to mitigate fibrotic diseases. Ginsenosides, the primary bioactive compounds in ginseng, have garnered significant attention. Over the past five years, extensive research has explored the pharmaceutical potential of ginsenosides in diverse organ fibrosis conditions, including liver, myocardial, renal, and pulmonary fibrosis. Studies have elucidated that ginsenosides demonstrate potential effects on inflammatory responses stemming from parenchymal cell damage, myofibroblast activation leading to extracellular matrix (ECM) production, and myofibroblast apoptosis or inactivation. Additionally, potential downstream targets and pathways associated with these pathological processes have been identified as being influenced by ginsenosides. This review presents a comprehensive overview of the efficacious treatments utilizing ginsenosides for various tissue fibrosis types and their potential anti-fibrotic mechanisms. Furthermore, it offers a reference for the development of novel candidate drugs for future organ fibrosis therapies.
