ArticleNature cardiovascular research2024
Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Mild oxidative stress and dietary epigenetic modulators direct DNA methylation remodeling toward stress-resilience pathways.BMC genomics · 2026Article
- A temporal dialogue between the circadian clock and chronic inflammatory diseases.Disease models & mechanisms · 2026Review
- Multidimensional regulation of hepatic macrophages in chronic liver disease: from metabolic reprogramming to intercellular and interorgan crosstalk.Frontiers in immunology · 2026Review
- Allogeneic haematopoietic cell transplantation promotes atherosclerosis in mice via CD8+ T cells.Cardiovascular research · 2025Article
- Clinical staging to guide management of metabolic disorders and their sequelae: a European Atherosclerosis Society consensus statement.European heart journal · 2025Article
- Targeting Liver Epsins Ameliorates Dyslipidemia in Atherosclerosis through Inhibition of Proprotein Convertase Subtilisin/Kexin Type 9-Mediated Low-density Lipoprotein Receptor Degradation.bioRxiv : the preprint server for biology · 2025Article
- Lipid Accumulation and Insulin Resistance: Bridging Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- Metabolic diseases and Kupffer cell's plasticity.Immunometabolism (Cobham, Surrey) · 2025Article
- Synergistic therapeutic strategies for metabolic dysfunction-associated steatohepatitis and type 2 diabetes mellitus: molecular insights and clinical advances.Frontiers in endocrinology · 2025Review
- Loss of embryonically-derived Kupffer cells during hypercholesterolemia accelerates atherosclerosis development.Nature communications · 2024Article
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21 authors.
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Abstract
Apolipoprotein-B (APOB)-containing lipoproteins cause atherosclerosis. Whether the vasculature is the initially responding site or if atherogenic dyslipidemia affects other organs simultaneously is unknown. Here we show that the liver responds to a dyslipidemic insult based on inducible models of familial hypercholesterolemia and APOB tracing. An acute transition to atherogenic APOB lipoprotein levels resulted in uptake by Kupffer cells and rapid accumulation of triglycerides and cholesterol in the liver. Bulk and single-cell RNA sequencing revealed a Kupffer-cell-specific transcriptional program that was not activated by a high-fat diet alone or detected in standard liver function or pathological assays, even in the presence of fulminant atherosclerosis. Depletion of Kupffer cells altered the dynamic of plasma and liver lipid concentrations, indicating that these liver macrophages help restrain and buffer atherogenic lipoproteins while simultaneously secreting atherosclerosis-modulating factors into plasma. Our results place Kupffer cells as key sentinels in organizing systemic responses to lipoproteins at the initiation of atherosclerosis.
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