ArticleHypertension (Dallas, Tex. : 1979)2024
Intact NOX2 in T Cells Mediates Pregnancy-Induced Renal Damage in Dahl SS Rats.
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Experimental Animal Models of Preeclampsia: Mechanisms, Strengths, and Translational Relevance.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Exacerbation of Dahl SS Hypertension and Renal Damage by NOX2 in CD4+ T Cells.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Impact of Hematopoietic CD14 on Oxidative Stress during Salt-Sensitive Hypertension and Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Oxidative Stress and Inflammation in Uterine-Vascular Adaptation During Pregnancy.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundHypertensive disorders of pregnancy are associated with increased risk for cardiovascular disease, renal disease, and mortality. While the exact mechanisms remain unclear, T cells and reactive oxygen species have been implicated in its pathogenesis. We utilized Dahl salt-sensitive (SS), SS
methodsWe assessed blood pressure and renal damage phenotypes in SS, SS
resultsMultigravida SS rats developed significant pregnancy-induced renal damage and renal functional impairment associated with elevated maternal mortality rates, whereas deletion of T cells or NOX2 garnered protection. During primigravida states, this attenuation in renal damage was observed, with the greatest protection in the SS
conclusionsT cells and NOX2-derived reactive oxygen species, thus, contribute to end-organ damage in both primigravida and multigravida pregnancies in the SS rat leading to increases in maternal mortality.
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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 Socratic graph.