ArticleRedox biology2026
Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
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Authors and funding
14 authors.
Funding
Abstract
Inflammation is a key factor in the development of heart failure (HF), with interleukin-12 (IL-12) and interleukin-23 (IL-23) acting as significant pro-inflammatory cytokines, both of which are simultaneously reduced by inhibiting IL-12β. This study utilized IL-12β knockout (KO) mice to investigate whether genetically inhibiting IL-12β could lessen transverse aortic constriction (TAC)-induced cardiac inflammation, hypertrophy, and dysfunction, as well as associated lung remodeling. We found that IL-12β KO significantly improved TAC-induced cardiac dysfunction in both male and female mice, evidenced by better left ventricular (LV) ejection fraction and fractional shortening. Additionally, IL-12β KO substantially reduced the TAC-induced increases in the weight of the LV, left atrium, lung, and right ventricle (RV), and their ratios to body weight or tibial length in both sexes. Furthermore, IL-12β KO markedly attenuated TAC-induced LV leukocyte infiltration, cardiomyocyte hypertrophy, fibrosis, and subsequent lung inflammation and remodeling. Bulk LV RNA sequencing demonstrated that IL-12β KO also mitigated TAC-induced changes in LV gene profiles linked to inflammation and fibrosis. We also found that IL-12β KO significantly reduced TAC-induced LV accumulation of various immune cell subsets, activation of CD4
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