ArticleActa pharmacologica Sinica2015
Involvement of endoplasmic reticulum stress in angiotensin II-induced NLRP3 inflammasome activation in human renal proximal tubular cells in vitro.
Article in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 67 citations in OpenAlex.
- Innate immunity and hypertension: unveiling inflammatory pathways for novel therapies.Frontiers in pharmacology · 2026Review
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- Natural products derived from traditional Chinese medicines targeting ER stress for the treatment of kidney diseases.Renal failure · 2024Review
- Artesunate Alleviates Kidney Fibrosis in Type 1 Diabetes with Periodontitis Rats via Promoting Autophagy and Suppression of Inflammation.ACS omega · 2024Article
- Role and mechanism of endoplasmic reticulum stress and NLRP3 inflammasome in acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Activation of the Nrf2/ARE signaling pathway ameliorates hyperlipidemia-induced renal tubular epithelial cell injury by inhibiting mtROS-mediated NLRP3 inflammasome activation.Frontiers in immunology · 2024Article
- Research progress on endoplasmic reticulum homeostasis in kidney diseases.Cell death & disease · 2023Review
- Adipolin protects against renal injury via PPARα-dependent reduction of inflammasome activation.iScience · 2023Article
- LncRNA MHRT Prevents Angiotensin II-Induced Myocardial Oxidative Stress and NLRP3 Inflammasome via Nrf2 Activation.Antioxidants (Basel, Switzerland) · 2023Article
- Role of ER Stress Mediated Unfolded Protein Responses and ER Stress Inhibitors in the Pathogenesis of Inflammatory Bowel Disease.Digestive diseases and sciences · 2022Review
- Epigallocatechin-3-gallate ameliorates renal endoplasmic reticulum stress-mediated inflammation in type 2 diabetic rats.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Immunosuppression by Mycophenolate Mofetil Mitigates Intrarenal Angiotensinogen Augmentation in Angiotensin II-Dependent Hypertension.International journal of molecular sciences · 2022Article
- Role of the renin-angiotensin system in NETosis in the coronavirus disease 2019 (COVID-19).Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Kidney Damage Caused by Obesity and Its Feasible Treatment Drugs.International journal of molecular sciences · 2022Review
- Endoplasmic reticulum as a target in cardiovascular diseases: Is there a role for flavonoids?Frontiers in pharmacology · 2022Review
- Cellular Senescence and Regulated Cell Death of Tubular Epithelial Cells in Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Therapeutic Approaches Targeting Proteostasis in Kidney Disease and Fibrosis.International journal of molecular sciences · 2021Review
- HDAC2 targeting stabilizes the CoREST complex in renal tubular cells and protects against renal ischemia/reperfusion injury.Scientific reports · 2021Article
- Attenuating Effects of Dieckol on Hypertensive Nephropathy in Spontaneously Hypertensive Rats.International journal of molecular sciences · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
aimNLRP3 inflammasome plays an important role in renal injury and may be a therapeutic target in the treatment of patients with progressive chronic kidney disease. In this study we investigated whether angiotensin II (Ang II)-induced NLRP3 inflammasome activation was linked to endoplasmic reticulum stress (ERS) in human renal proximal tubular cells in vitro.
methodsHuman kidney proximal epithelial cells (HK-2) were pretreated with telmisartan or 4-PBA, and then treated with Ang II. The expression levels of mRNAs and proteins related to NLRP3 inflammasomes and ERS was examined by real-time PCR, Western blot and immunofluorescence.
resultsTreatment with Ang II (10, 100, and 1000 nmol/L) increased the expression of the inflammasome markers NLRP3 and ASC, as well as caspase-1, IL-1β, and IL-18 in dose- and time-dependent manners with peak levels detected at 100 nmol/L and 12 h. Ang II-induced increases in the expression of NLRP3, ASC, caspase-1, IL-1β, and IL-18 were significantly reduced by pretreatment with telmisartan (1 μmol/L). Immunofluorescence studies showed that Ang II increased the expression of NLRP3 and ASC, which was inhibited by telmisartan. Furthermore, Ang II treatment increased the expression of ERS markers GRP78 and p-eIF2α in dose- and time-dependent manners, which was significantly reduced by telmisartan. Moreover, Ang II-induced increases in the expression of NLRP3, ASC, caspase-1, IL-1β, and IL-18 were significantly inhibited by pretreatment with the ERS inhibitor 4-PBA (5 mmol/L).
conclusionAng II treatment induces NLRP3 inflammasome activation in HK-2 cells in vitro and ER stress is involved in this process, which may represent a new mechanism for the renal rennin-angiotensin system to induce tubulointerstitial inflammation.
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