ArticleClinical and experimental nephrology2025
Pharmacological inhibition of the NLRP3 inflammasome attenuates kidney apoptosis, fibrosis, and injury in Dahl salt-sensitive rats.
Article in Clinical and experimental nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- The Inflammatory Cell Death in Diabetic Kidney Disease: Integrating Multifactorial Mechanisms into Novel Therapeutics.International journal of molecular sciences · 2025Review
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Abstract
backgroundSalt-sensitive hypertension (SSH) is the most severe form of hypertension, and the presence of NLRP3 inflammasome plays a crucial role in its pathogenesis. Although MCC950 has shown therapeutic potential for hypertension and kidney injury, its mechanism of action remains unclear.
methodsDahl salt-sensitive (SS) rats and their salt-tolerant aptamer control SS-13
resultsCompared with the SS + vehicle group, the SS + MCC950 group showed significantly lower blood pressure levels. Additionally, inhibition of NLRP3 inflammasome activation was observed along with reduced inflammation, apoptosis, fibrosis, and sodium retention in the kidneys.
conclusionsThe findings suggest that pharmacological inhibition of the NLRP3 inflammasome reduces blood pressure in SS rats and alleviates related kidney injury by suppressing inflammation, apoptosis, fibrosis, and sodium retention.
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