ArticleBritish journal of pharmacology2016
Endothelin-1 contributes to the progression of renal injury in sickle cell disease via reactive oxygen species.
Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Association between diffuse myocardial fibrosis and diastolic dysfunction in sickle cell anemia.Blood · 2017Trial
- Natural History of Chronic Kidney Disease in Sickle Cell Disease.American journal of hematology · 2026Review
- Review
- Endothelin receptor antagonism in sickle cell disease: Is the time now?Canadian journal of physiology and pharmacology · 2026Review
- Emerging pathways in thromboinflammation of sickle cell disease: novel findings in disease pathogenesis.Research and practice in thrombosis and haemostasis · 2025Review
- End Organ Affection in Sickle Cell Disease.Cells · 2024Review
- Article
- Sickle Cell Disease and CKD: An Update.American journal of nephrology · 2024Review
- NLRP3 activation contributes to endothelin-1-induced erectile dysfunction.Journal of cellular and molecular medicine · 2023Article
- Endothelin system expression in the kidney following cisplatin-induced acute kidney injury in male and female mice.Canadian journal of physiology and pharmacology · 2022Article
- Endothelin A receptor antagonist attenuated renal iron accumulation in iron overload heme oxygenase-1 knockout mice.Canadian journal of physiology and pharmacology · 2022Article
- The nephropathy of sickle cell trait and sickle cell disease.Nature reviews. Nephrology · 2022Review
- Hydroxyurea improves nitric oxide bioavailability in humanized sickle cell mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- The Worst Things in Life are Free: The Role of Free Heme in Sickle Cell Disease.Frontiers in immunology · 2020Review
- Genetic polymorphisms associated with reactive oxygen species and blood pressure regulation.The pharmacogenomics journal · 2019Review
- Combined hydroxyurea and ETActa physiologica (Oxford, England) · 2019Article
- Effect of renin-angiotensin-aldosterone system blocking agents on progression of glomerulopathy in sickle cell disease.British journal of haematology · 2019Observational
- Risk factors for hypertensive retinopathy in a Chinese population with hypertension: The Beijing Eye study.Experimental and therapeutic medicine · 2019Article
- Endothelin type A receptors mediate pain in a mouse model of sickle cell disease.Haematologica · 2018Article
- Sickle cell nephropathy: an update on pathophysiology, diagnosis, and treatment.International urology and nephrology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
background and purposeEndothelin-1 (ET-1) is increased in patients with sickle cell disease and may contribute to the development of sickle cell nephropathy. The current study was designed to determine whether ET-1 acting via the ETA receptor contributes to renal injury in a mouse model of sickle cell disease. EXPERIMENTAL APPROACH: Adult, humanized HbSS (homozygous for sickle Hb) mice had increased ET-1 mRNA expression in both the cortex and the glomeruli compared with mice heterozygous for sickle and Hb A (HbAS controls). In the renal cortex, ETA receptor mRNA expression was also elevated in HbSS (sickle) mice although ETB receptor mRNA expression was unchanged. Ligand binding assays confirmed that sickle mice had increased ETA receptors in the renal vascular tissue when compared with control mice. KEY
resultsIn response to PKC stimulation, reactive oxygen species production by isolated glomeruli from HbSS sickle mice was increased compared with that from HbSA controls, an effect that was prevented by 1 week in vivo treatment with the selective ETA antagonist, ABT-627. Protein and nephrin excretion were both elevated in sickle mice, effects that were also significantly attenuated by ABT-627. Finally, ETA receptor antagonism caused a significant reduction in mRNA expression of NADPH oxidase subunits, which may contribute to nephropathy in sickle cell disease. CONCLUSIONS AND IMPLICATIONS: These data support a novel role for ET-1 in the progression of sickle nephropathy, specifically via the ETA receptor, and suggest a potential role for ETA receptor antagonism in a treatment strategy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.