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Dietary cholesterol, rather than liver steatosis, leads to hepatic inflammation in hyperlipidemic mouse models of nonalcoholic steatohepatitis
TLDR
Findings indicate that dietary cholesterol, possibly in the form of modified plasma lipoproteins, is an important risk factor for the progression to hepatic inflammation in diet‐induced NASH.
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LDL Receptor Knock-Out Mice Are a Physiological Model Particularly Vulnerable to Study the Onset of Inflammation in Non-Alcoholic Fatty Liver Disease
TLDR
The Ldlr−/− mice are a promising physiological model particularly vulnerable for investigating the onset of hepatic inflammation in non-alcoholic steatohepatitis and developed sustained liver damage upon long term HFC feeding due to increased sensitivity for oxLDL uptake.
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Roles of PPARs in NAFLD: potential therapeutic targets.
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Functional genomics of the CDKN2A/B locus in cardiovascular and metabolic disease: what have we learned from GWASs?
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Macrophage MicroRNA-155 Promotes Cardiac Hypertrophy and Failure
TLDR
The findings reveal that microRNA-155 expression in macrophages promotes cardiac inflammation, hypertrophy, and failure in response to pressure overload, which supports the causative significance of inflammatory signaling in hypertrophic heart disease and demonstrates the feasibility of therapeutic microRNA targeting of inflammation in heart failure.
View on Wolters Kluwer
Internalization of Modified Lipids by CD36 and SR-A Leads to Hepatic Inflammation and Lysosomal Cholesterol Storage in Kupffer Cells
TLDR
CD36 and MSR1 contribute similarly and independently to the progression of inflammation in NASH, by affecting intracellular cholesterol distribution inside Kupffer cells (KCs).
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Human Adipose Tissue Macrophages Display Activation of Cancer-related Pathways*
TLDR
Whether human adipose tissue macrophages (ATM) modulate cancer cell function is studied and it is shown that the concentrations of ATM-secreted factors related to cancer are elevated in serum of obese subjects, suggesting that ATM may modulate the cancer cell phenotype.
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Higher levels of advanced glycation endproducts in human carotid atherosclerotic plaques are associated with a rupture-prone phenotype.
TLDR
This is the first study showing that AGEs are associated with human rupture-prone plaques and suggests a cascade linking inflammation, reduced GLO-1, methylglyoxal- and AGE-accumulation, and subsequent apoptosis.
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Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates.
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Understanding hyperlipidemia and atherosclerosis: lessons from genetically modified apoe and ldlr mice
TLDR
This review focuses on the use of two of the most widely used mouse models, ApoE- and LDLR-deficient mice, and elaborate on mice expressing mutant forms of APOE, including the APOE3Leiden (APOE3L) and the APoe2 knock-in ( APOE2k) mouse models.
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