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Updated: Jun 30, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
The role of PI3K/Akt signaling pathway in chronic kidney disease
Hongshuang Wang1, Lanjun Gao1, Chenchen Zhao1
1Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Insights
Targeting the phosphatidylinositol 3-kinases (PI3K)/protein kinase B (Akt) pathway shows promise for treating chronic kidney disease (CKD). Modulating this pathway may reduce kidney damage by impacting inflammation, apoptosis, and autophagy.
Area of Science:
- Nephrology
- Molecular Biology
- Pharmacology
Background:
- Chronic kidney disease (CKD) encompasses conditions like glomerulonephritis, IgA nephropathy, and diabetic nephropathy, marked by kidney structural damage and functional decline.
- Current CKD treatments focus on symptom management, lacking disease-modifying therapies.
- The phosphatidylinositol 3-kinases (PI3K)/protein kinase B (Akt) signaling pathway is implicated in CKD pathogenesis.
Purpose of the Study:
- To review the role of the PI3K/Akt pathway in CKD-related inflammation, apoptosis, autophagy, and epithelial-mesenchymal transition (EMT).
- To summarize current evidence on targeting the PI3K/Akt pathway for CKD treatment.
- To identify research gaps and challenges in developing PI3K/Akt-targeted CKD therapies.
Main Methods:
- Literature review of studies investigating the PI3K/Akt pathway in CKD.
- Analysis of preclinical and clinical data on PI3K/Akt modulators in CKD models.
- Synthesis of information on the pathway's involvement in key pathological processes.
Main Results:
- The PI3K/Akt pathway significantly influences inflammation, oxidative stress, apoptosis, autophagy, and EMT in CKD.
- Inhibiting or activating specific components of the PI3K/Akt pathway can ameliorate kidney damage.
- Emerging therapeutic strategies focus on modulating this pathway for CKD treatment.
Conclusions:
- The PI3K/Akt pathway is a critical regulator of CKD progression and a potential therapeutic target.
- Further research is needed to overcome challenges in translating PI3K/Akt-targeted therapies into clinical practice for CKD.
- Developing effective CKD treatments requires a deeper understanding of PI3K/Akt pathway modulation.
Abstract:
Chronic kidney disease (CKD), including chronic glomerulonephritis, IgA nephropathy and diabetic nephropathy, are common chronic diseases characterized by structural damage and functional decline of the kidneys. The current treatment of CKD is symptom relief. Several studies have reported that the phosphatidylinositol 3 kinases (PI3K)/protein kinase B (Akt) signaling pathway is a pathway closely related to the pathological process of CKD. It can ameliorate kidney damage by inhibiting this signal pathway which is involved with inflammation, oxidative stress, cell apoptosis, epithelial mesenchymal transformation (EMT) and autophagy. This review highlights the role of activating or inhibiting the PI3K/Akt signaling pathway in CKD-induced inflammatory response, apoptosis, autophagy and EMT. We also summarize the latest evidence on treating CKD by targeting the PI3K/Akt pathway, discuss the shortcomings and deficiencies of PI3K/Akt research in the field of CKD, and identify potential challenges in developing these clinical therapeutic CKD strategies, and provide appropriate solutions.
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