ArticleFrontiers in cell and developmental biology2020
Contribution of TGF-Beta-Mediated NLRP3-HMGB1 Activation to Tubulointerstitial Fibrosis in Rat With Angiotensin II-Induced Chronic Kidney Disease.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 242 citations in OpenAlex.
- THBS1 inhibition alleviates inflammatory response by inhibiting TGF-β and NLRP3 inflammasome in experimental murine dry eye.Medical molecular morphology · 2026Article
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- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- Resveratrol glycoside inhibits NLRP3/IL-1β/NF-κB to alleviate peritoneal fibrosis in peritoneal dialysis.Clinical and experimental nephrology · 2025Article
- Multi-Target Modulation of Polyphenols in Diabetic Kidney Disease Therapeutics: A Comprehensive Review.Food science & nutrition · 2025Review
- Decoding diabetic kidney disease: a comprehensive review of interconnected pathways, molecular mediators, and therapeutic insights.Diabetology & metabolic syndrome · 2025Review
- Semaglutide and adenosine alleviate obesity-induced kidney injury, with observed modulation of the Txnip/NLRP3 pathway.Diabetology & metabolic syndrome · 2025Article
- Ras Guanine Nucleotide-Releasing Protein-4 Inhibits Erythropoietin Production in Diabetic Mice with Kidney Disease by Degrading HIF2A.Diabetes & metabolism journal · 2025Article
- Clinical Trial: Effects of Autologous Dendritic Cell Administration on Renal Hemodynamics and Inflammatory Biomarkers in Diabetic Kidney Disease.Diseases (Basel, Switzerland) · 2025Article
- Therapeutic potential of synthetic and natural iron chelators against ferroptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Involvement of role of HMGB1-NLRP3 pathway in systemic disorders.Frontiers in cell and developmental biology · 2025Review
- Article
- Ferroptosis and Its Potential Role in the Physiopathology of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- High mobility group box 1 (HMGB1) is a potential disease biomarker in cell and mouse models of Duchenne muscular dystrophy.Biology open · 2024Article
- Statin administration or blocking PCSK9 alleviates airway hyperresponsiveness and lung fibrosis in high-fat diet-induced obese mice.Respiratory research · 2024Article
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Effects of acute- and long-term aerobic exercises at different intensities on bone in mice.Journal of bone and mineral metabolism · 2024Article
- Linking NLRP3 inflammasome and pulmonary fibrosis: mechanistic insights and promising therapeutic avenues.Inflammopharmacology · 2024Review
- The impact of ferroptosis and ferroptosis-related non-coding RNAs on breast cancer progression.Frontiers in cell and developmental biology · 2024Review
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11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is a common phenotype that often leads to the progression of blood pressure-induced chronic kidney disease (CKD). TGF-beta plays an important role in promoting pathogenesis, and NLRP3 is a critical mediator in the progression of blood pressure-induced CKD. However, the pathophysiological roles of the TGF-beta-mediated NLRP3 pathway in modulating fibrosis in blood pressure-induced CKD have not been elucidated. The present study aims to investigate the contribution of TGF-beta-mediated NLRP3 inflammasome to renal fibrosis in rats with high blood pressure. By treating rats with angiotensin II (Ang II) for 14 days, we observed the development of fibrosis, characterized by epithelial-mesenchymal transition (EMT) markers [alpha-smooth muscle actin (alpha-SMA), MMP-2, and MMP-9]. Immunohistochemical analysis further revealed that TGF-beta and NLRP3 inflammasome activation [high-mobility group box 1 (HMGB1), IL-1beta, and NLRP3] were significantly upregulated in the kidney of rats with Ang II-induced hypertension. Interestingly, we observed that Ang II could not increase the production of NLRP3 proteins, but TGF-beta could induce NLRP3 protein expression in cultured NRK-52E cells. Furthermore, we speculated that TGF-beta played a pathogenic role in Ang II-induced CKD because TGF-beta induced the activation of NLRP3 inflammasomes and Gasdermin D cleavage expression. We also proved that the pharmacological inhibition of NLRP3 by ISO caused a decrease in TGF-beta-induced NLRP3 inflammasome activation and the expression of EMT markers (alpha-SMA and CollagenI) and Gasdermin D cleavage. Collectively, these results suggest that TGF-beta-mediated NLRP3 inflammasome activation may cause the release of HMGB1 and an increase in Gasdermin D cleavage in NRK-52E, thereby contributing to renal fibrosis in Ang II-induced CKD. These findings provide novel insights into the pathogenic role of NLRP3 in CKD associated with high blood pressure.
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