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Review Article

Advances in Traditional Chinese Medicine research in diabetic kidney disease treatment

, , , , , & show all
Pages 222-232 | Received 30 Aug 2023, Accepted 31 Jan 2024, Published online: 15 Feb 2024

Figures & data

Figure 1. DKD is primarily caused by a number of interconnected mechanisms, including excessive filtration damage to the GFB, dilatation, and oxidation of the glomerular mesangium. These mechanisms are complex in nature, with links to hemodynamics, metabolism, and immunopathology. The physiological mechanism of DKD is summarized in this diagram.

Figure 1. DKD is primarily caused by a number of interconnected mechanisms, including excessive filtration damage to the GFB, dilatation, and oxidation of the glomerular mesangium. These mechanisms are complex in nature, with links to hemodynamics, metabolism, and immunopathology. The physiological mechanism of DKD is summarized in this diagram.

Table 1. Clinical studies on the efficacy of prescription formulas in the treatment of DKD.

Figure 2. AS-IV may treat DKD by reducing inflammation, attenuating ERS, regulating calcium homeostasis, restoring mitochondrial homeostasis (via the Drp-1 and PINK1/Parkin signaling pathways), countering oxidative stress, and improving EMT and vascular endothelial function.

Figure 2. AS-IV may treat DKD by reducing inflammation, attenuating ERS, regulating calcium homeostasis, restoring mitochondrial homeostasis (via the Drp-1 and PINK1/Parkin signaling pathways), countering oxidative stress, and improving EMT and vascular endothelial function.

Figure 3. ROS, ATP and other substances trigger NF-κB dependent pro-IL-1β and pro-IL-18 gene transcription by activating TLR/IL-1 receptors. After Caspase-1 cleavage, these pro-inflammatory factors are released into the cytoplasm in the form of pro-IL-1β and pro-IL-18, thus participating in the inflammatory response.

Figure 3. ROS, ATP and other substances trigger NF-κB dependent pro-IL-1β and pro-IL-18 gene transcription by activating TLR/IL-1 receptors. After Caspase-1 cleavage, these pro-inflammatory factors are released into the cytoplasm in the form of pro-IL-1β and pro-IL-18, thus participating in the inflammatory response.

Data availability statement

This review uses data from a variety of sources, including PubMed, Cochrane Library, VIP, Wanfang Data, CNKI, and CBM, etc.