ArticleFrontiers in immunology2023
Inhibition of NK1.1 signaling attenuates pressure overload-induced heart failure, and consequent pulmonary inflammation and remodeling.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.Redox biology · 2026Article
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- PHD2 Deletion in CD8Hypertension (Dallas, Tex. : 1979) · 2025Article
- Translational Insights into NK Immunophenotyping: Comparative Surface Marker Analysis and Circulating Immune Cell Profiling in Cancer Immunotherapy.International journal of molecular sciences · 2025Review
- Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac inflammation and heart failure development.bioRxiv : the preprint server for biology · 2025Article
- Article
- Lymphocyte to c-reactive protein ratio predicts the risk of contrast-induced acute kidney injury in STEMI patients undergoing percutaneous coronary intervention.BMC cardiovascular disorders · 2025Article
- Pharmacological inhibition of IL12β is effective in treating pressure overload-induced cardiac inflammation and heart failure.Frontiers in immunology · 2025Article
- Myocardial Inflammation in Heart Failure With Reduced and Preserved Ejection Fraction.Circulation research · 2024Review
- CD8 T cells promote heart failure progression in mice with preexisting left ventricular dysfunction.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Background: Inflammation contributes to heart failure (HF) development, the progression from left ventricular failure to pulmonary remodeling, and the consequent right ventricular hypertrophy and failure. NK1.1 plays a critical role in Natural killer (NK) and NK T (NKT) cells, but the role of NK1.1 in HF development and progression is unknown. Methods: We studied the effects of NK1.1 inhibition on transverse aortic constriction (TAC)-induced cardiopulmonary inflammation, HF development, and HF progression in immunocompetent male mice of C57BL/6J background. Results: We found that NK1.1 Conclusions: Our data suggest that inhibition of NK1.1 signaling is effective in attenuating systolic overload-induced cardiac fibrosis, dysfunction, and consequent pulmonary remodeling in immunocompetent mice through modulating the cardiopulmonary inflammatory response.
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What OpenQuestion holds
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.