Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Jun 13:13:900491.
doi: 10.3389/fphar.2022.900491. eCollection 2022.

Research Progress of Chinese Herbal Medicine Intervention in Renal Interstitial Fibrosis

Affiliations
Review

Research Progress of Chinese Herbal Medicine Intervention in Renal Interstitial Fibrosis

Xiao-Yuan Liu et al. Front Pharmacol. .

Abstract

Chronic kidney diseases usually cause renal interstitial fibrosis, the prevention, delay, and treatment of which is a global research hotspot. However, no definite treatment options are available in modern medicine. Chinese herbal medicine has a long history, rich varieties, and accurate treatment effects. Hitherto, many Chinese herbal medicine studies have emerged to improve renal interstitial fibrosis. This paper reviews the mechanisms of renal interstitial fibrosis and recent studies on the disease intervention with Chinese herbal medicine through literature search, intend to reveal the importance of Chinese herbal medicine in renal interstitial fibrosis. The results show that Chinese herbal medicine can improve renal interstitial fibrosis, and the effects of Chinese herbal medicine on specific pathological mechanisms underlying renal interstitial fibrosis have been explored. Additionally, the limitations and advantages of Chinese herbal medicine in the treatment of renal interstitial fibrosis, possible research directions, and new targets of Chinese herbal medicine are discussed to provide a basis for studies of renal interstitial fibrosis.

Keywords: Chinese herbal medicine; chronic kidney disease; mechanism; renal interstitial fibrosis; research progress.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Pathological factors in renal interstitial fibrosis. Excessive deposition of extracellular matrix (ECM) is the main cause of renal interstitial fibrosis. Epithelial-mesenchymal transition (EMT) refers to the phenotypic transformation of epithelial cells to fibroblast-like cells by acquiring a mesenchymal morphology, through decreased expression of E-cadherin and increased expression of N-cadherin. The proliferation of fibroblasts is the precursor of ECM overproduction. The factors promoting/inhibiting fibrosis restrict each other, and the dynamic balance is lost, leading to the formation of fibrosis. The damaged part of renal interstitium can be rapidly infiltrated by a large number of inflammatory cells, aggravating fibrosis. The abnormal increase in reactive oxygen species (ROS) generation during oxidative stress can directly induce pathological damage to various renal cells and reduce the degradation of ECM by mesangial cells. On the other hand, ROS can participate in intracellular signaling pathways as a signaling molecule, causing RIF.

References

    1. Bai L., Huo B., Chen Z., Guo Q., Xu J., Fang J., et al. (2017a). Effect of Huayu Tongluo Herbs on Reduction of Proteinuria via Inhibition of Wnt/β-Catenin Signaling Pathway in Diabetic Rats. Evid. Based Complement. Altern. Med. 2017, 3054145. 10.1155/2017/3054145 - DOI - PMC - PubMed
    1. Bai Y., Wu C., Hong W., Zhang X., Liu L., Chen B. (2017b). Anti-Fibrotic Effect of Sedum Sarmentosum Bunge Extract in Kidneys via the Hedgehog Signaling Pathway. Mol. Med. Rep. 16, 737–745. 10.3892/mmr.2017.6628 - DOI - PMC - PubMed
    1. Barkett M., Gilmore T. D. (1999). Control of Apoptosis by Rel/NF-kappaB Transcription Factors. Oncogene 18, 6910–6924. 10.1038/sj.onc.1203238 - DOI - PubMed
    1. Basak S., Behar M., Hoffmann A. (2012). Lessons from Mathematically Modeling the NF-κB Pathway. Immunol. Rev. 246, 221–238. 10.1111/j.1600-065X.2011.01092.x - DOI - PMC - PubMed
    1. Bitzer M., von Gersdorff G., Liang D., Dominguez-Rosales A., Beg A. A., Rojkind M., et al. (2000). A Mechanism of Suppression of TGF-Beta/SMAD Signaling by NF-Kappa B/RelA. Genes Dev. 14, 187–197. 10.1101/gad.14.2.187 - DOI - PMC - PubMed

LinkOut - more resources