ArticleActa pharmacologica Sinica2022
Pharmacological inhibition of MyD88 suppresses inflammation in tubular epithelial cells and prevents diabetic nephropathy in experimental mice.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 28 citations in OpenAlex.
- Mogroside V Alleviates Renal Injury in Diabetic Mice via Regulation of theInternational journal of molecular sciences · 2026Article
- Inhibition of MyD88 in Tubular Epithelial Cells Alleviates the Cellular Senescence in Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- PCSK9 Inhibitors: A Potential Priority Choice for Lipid Management in Patients with Diabetic Kidney Disease.Drugs · 2025Review
- Renoprotective mechanisms of celastrol in high glucose-mediated HK-2 cell injury through inhibition of the PI3K/Akt/NF-κB signalling pathway.Biochemistry and biophysics reports · 2025Article
- Pharmacological targeting of adaptor proteins in chronic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Research Progress of Pyroptosis in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- MyD88 and Its Inhibitors in Cancer: Prospects and Challenges.Biomolecules · 2024Review
- Protective effect of modified Huangqi Chifeng decoction on immunoglobulin A nephropathy through toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Biochanin A Ameliorates Nephropathy in High-Fat Diet/Streptozotocin-Induced Diabetic Rats: Effects on NF-kB/NLRP3 Axis, Pyroptosis, and Fibrosis.Antioxidants (Basel, Switzerland) · 2023Article
- Danzhi Jiangtang capsule reduces renal injury in rats with diabetes induced by high fat diet and streptozotocin downregulating toll-like receptor 4-nuclear factor-κB pathway and apoptosis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Relevance of the pyroptosis-related inflammasome drug targets in the Chuanxiong to improve diabetic nephropathy.Molecular medicine (Cambridge, Mass.) · 2022Article
- Long Noncoding RNA MEG3-205/Let-7a/MyD88 Axis Promotes Renal Inflammation and Fibrosis in Diabetic Nephropathy.Kidney diseases (Basel, Switzerland) · 2022Article
- A Glimpse of Inflammation and Anti-Inflammation Therapy in Diabetic Kidney Disease.Frontiers in physiology · 2022Review
- Aggravated renal fibrosis is positively associated with the activation of HMGB1-TLR2/4 signaling in STZ-induced diabetic mice.Open life sciences · 2022Article
- Serum LINC00861: A novel biomarker for diabetic nephropathy diagnosis and a promoter of renal injury via miR-378a-3p.Diabetes & vascular disease researchArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence shows that chronic inflammation mediated by toll-like receptors (TLRs) contributes to diabetic nephropathy. Myeloid differentiation primary-response protein-88 (MyD88) is an essential adapter protein of all TLRs except TLR3 in innate immunity. It is unclear whether MyD88 could be a therapeutic target for diabetic nephropathy. Here, we used a new small-molecule MyD88 inhibitor, LM8, to examine the pharmacological inhibition of MyD88 in protecting kidneys from inflammatory injury in diabetes. We showed that MyD88 was significantly activated in the kidney of STZ-induced type 1 diabetic mice in tubular epithelial cells as well as in high glucose-treated rat tubular epithelial cells NRK-52E. In cultured tubular epithelial cells, we show that LM8 (2.5-10 μM) or MyD88 siRNA attenuated high-concentration glucose-induced inflammatory and fibrogenic responses through inhibition of MyD88-TLR4 interaction and downstream NF-κB activation. Treatment with LM8 (5, 10 mg/kg, i.g.) significantly reduced renal inflammation and fibrosis and preserved renal function in both type 1 and type 2 diabetic mice. These renoprotective effects were associated with reduced MyD88-TLR4 complex formation, suppressed NF-κB signaling, and prevention of inflammatory factor expression. Collectively, our results show that hyperglycemia activates MyD88 signaling cascade to induce renal inflammation, fibrosis, and dysfunction. Pharmacological inhibition of MyD88 may be a therapeutic approach to mitigate diabetic nephropathy and the inhibitor LM8 could be a potential candidate for such therapy.
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