ArticleHypertension (Dallas, Tex. : 1979)2010
Tumor necrosis factor-alpha antagonist etanercept decreases blood pressure and protects the kidney in a mouse model of systemic lupus erythematosus.
Article in Hypertension (Dallas, Tex. : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 151 citations in OpenAlex.
- Engineering Murine Cross-Reactivity Into an Affibody to Human Death Receptor 5.Biotechnology and bioengineering · 2026Article
- Inflammatory factors and hypertensive nephropathy: A bidirectional 2-sample Mendelian randomization study.Medicine · 2026Article
- Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025Review
- Perinatal Exposure of Dams to a High Salt Diet Impaired Vascular Function and Elevated Biomarkers of Inflammation in the Offspring.Clinical Medicine Insights. Cardiology · 2025Article
- A Novel Preclinical Murine Model of Systemic Lupus Erythematosus-Like Cardiovascular Disease.ACR open rheumatology · 2024Article
- Implications of pregnancy on cardiometabolic disease risk: preeclampsia and gestational diabetes.American journal of physiology. Cell physiology · 2024Review
- Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024Review
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Mechanisms of inflammation modulation by different immune cells in hypertensive nephropathy.Frontiers in immunology · 2024Review
- Serum Isolevuglandin IgG Antibody Concentrations Are Increased in Patients with Systemic Lupus Erythematosus and Associated with Lower 24-Hour Blood Pressure.Frontiers in lupus · 2024Article
- A new immune disease: systemic hypertension.Clinical kidney journal · 2023Review
- Th1-related transcription factors and cytokines in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- A song of AAs and fire: divergent sex-dependent renal inflammatory mechanisms in hypertensive SLE mice.American journal of physiology. Heart and circulatory physiology · 2023Article
- Renal TLR-7/TNF-α pathway as a potential female-specific mechanism in the pathogenesis of autoimmune-induced hypertension.American journal of physiology. Heart and circulatory physiology · 2022Article
- Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.Hypertension (Dallas, Tex. : 1979) · 2022Review
- The Immune System in Hypertension: a Lost Shaker of Salt 2021 Lewis K. Dahl Memorial Lecture.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Treatment of male and female spontaneously hypertensive rats with TNF-α inhibitor etanercept increases markers of renal injury independent of an effect on blood pressure.Biology of sex differences · 2022Article
- Should Renal Inflammation Be Targeted While Treating Hypertension?Frontiers in physiology · 2022Review
- Therapeutic targeting of inflammation in hypertension: from novel mechanisms to translational perspective.Cardiovascular research · 2021Review
- Autoimmune-mediated renal disease and hypertension.Clinical science (London, England : 1979) · 2021Review
39 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Chronic inflammation has been implicated in the pathology of hypertension; however, the role for specific cytokines remains unclear. We tested whether tumor necrosis factor-α blockade with etanercept (Etan) reduces mean arterial pressure in a female mouse model of systemic lupus erythematosus (SLE). SLE is a chronic inflammatory disorder with prevalent hypertension. Thirty-week-old SLE (NZBWF1) and control mice (NZW/LacJ) received Etan (0.8 mg/kg SC weekly) for 4 weeks or vehicle. Mean arterial pressure (in millimeters of mercury) was increased in SLE mice (150±5 versus 113±5 in controls; P<0.05) and was lower in Etan-treated SLE mice (132±3) but not controls (117±5). Albuminuria (in micrograms per milligram of creatinine) was elevated in SLE mice (28 742±9032 versus 1075±883; P<0.05) and was lower in Etan-treated SLE mice (8154±3899) but not control animals (783±226). Glomerulosclerosis (in percentage of glomeruli) was evident in SLE mice (2.5±1.6 versus 0.0±0.0 in controls; P<0.05) and was ameliorated in Etan-treated SLE mice (0.1±0.1). Renal cortex CD68(+) cell staining (in percentage of area) was elevated in SLE mice (4.75±0.80 versus 0.79±0.12 in controls; P<0.05) and was lower in Etan-treated SLE mice (2.28±0.32) but not controls (1.43±0.25). Renal cortex NADPH oxidase activity (relative light units per milligram of protein) was higher in SLE mice compared with controls (10 718±1276 versus 7584±229; P<0.05) and lowered in Etan-treated SLE mice (6645±490). Renal cortex nuclear factor κB (phosphorylated and nonphosphorylated) was increased in SLE mice compared with controls and lower in Etan-treated SLE mice. These data suggest that TNF-α mechanistically contributes to the development of hypertension in a chronic inflammatory disease through increased renal nuclear factor κB, oxidative stress, and inflammation.
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