ArticleJournal of applied physiology (Bethesda, Md. : 1985)2025
Elevated LDL-C induces T-cell metabolic dysfunction and increases inflammation and oxidative stress in midlife adults.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- The influence of blood lipids on cerebral perfusion by apolipoprotein E status.Journal of lipid research · 2026Article
- Association of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) with cardiovascular mortality in peritoneal dialysis patients: a prospective cohort study.Frontiers in nutrition · 2026Article
- Bioinformatics analysis and qRT-PCR validation of iron metabolism-related genes in pediatric asthma.PloS one · 2026Article
- Association between NHHR and endometriosis and the mediating role of the CALLY index: a cross-sectional study based on NHANES.BMC women's health · 2025Article
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7 authors.
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Abstract
T-cells may contribute to chronic, low-grade, sustained inflammation and oxidative stress commonly observed with aging and chronic disease. T-cell metabolic alterations impact T-cell differentiation, inflammation, and oxidative stress in animal models. Low-density lipoprotein cholesterol (LDL-C) has been identified as a novel antigen that activates T-cells via a canonical pathway. However, in humans, little is known about the direct effect of LDL-C on T-cells. Endogenous LDL-C concentration peaks during midlife in humans and may contribute to midlife chronic disease risk by inducing T-cell dysfunction. Thus, this study investigated the effects of exogenous LDL-C exposure on CD4
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