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MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment
TLDR
Targeting MIF in individuals with manifest atherosclerosis can potentially be used to treat this condition and displays chemokine-like functions and acts as a major regulator of inflammatory cell recruitment and atherogenesis. Expand
Intracellular action of the cytokine MIF to modulate AP-1 activity and the cell cycle through Jab1
TLDR
It is concluded that MIF may act broadly to negatively regulate Jab1-controlled pathways and that the MIF–Jab1 interaction may provide a molecular basis for key activities of MIF. Expand
Mouse models for atherosclerosis and pharmaceutical modifiers.
TLDR
The mouse is the most useful, economic, and valid model for studying atherosclerosis and exploring effective therapeutic approaches and the choice of a model should take into account the risk factor to be studied and the working spectrum of the compounds tested. Expand
The Direct Peroxisome Proliferator-activated Receptor Target Fasting-induced Adipose Factor (FIAF/PGAR/ANGPTL4) Is Present in Blood Plasma as a Truncated Protein That Is Increased by Fenofibrate
TLDR
Levels of both truncated and native FIAF showed marked interindividual variation but were not associated with body mass index and were not influenced by prolonged semistarvation, suggesting that FIAF, similar to other adipocytokines such as adiponectin, may partially exert its function via a truncated form. Expand
Cytokines and atherosclerosis: a comprehensive review of studies in mice
TLDR
This survey summarizes the currently available information from mouse studies on the contribution of a specified group of cytokines expressed in atherosclerotic lesions and concludes that only for a few cytokines there is sufficient consistent data allowing classifying them as typically proatherogenic (IL-1,IL-12, IL-18, MIF, IFN-γ, TNF-α, and M-CSF) or anti-atherogensic ( IL-10). Expand
Disulfide analysis reveals a role for macrophage migration inhibitory factor (MIF) as thiol-protein oxidoreductase.
TLDR
It is argued that MIF exhibits enzymatic oxidoreductase activity, that this activity is dependent on the presence of the catalytic center that is formed by cysteine residues 57 and 60, and that certain MIF-mediated immune processes are due to the Cysteine-mediated redox mechanism. Expand
Macrophage migration inhibitory factor (MIF): mechanisms of action and role in disease.
TLDR
This work attempts to correlate current knowledge on the molecular pathways of MIF activity with its functions in immunity and disease. Expand
Collagen degradation in the abdominal aneurysm: a conspiracy of matrix metalloproteinase and cysteine collagenases.
TLDR
Signs are found that a secondary deficiency in abdominal aortic aneurysms relates to cystatin C degradation by (neutrophil-derived) proteases, and the presence of the osteoclastic proton pump indicated optimal conditions for extracellular cysteine protease activity. Expand
Global Suppression of IL-6-induced Acute Phase Response Gene Expression after Chronic in Vivo Treatment with the Peroxisome Proliferator-activated Receptor-α Activator Fenofibrate*
TLDR
It is demonstrated that chronic treatment with the PPARα agonist fenofibrate fully prevents the IL-6-induced APR gene expression in wild-type but not in PPAR α-deficient mice. Expand
Time-Resolved and Tissue-Specific Systems Analysis of the Pathogenesis of Insulin Resistance
TLDR
HFD-induced IR is a time- and tissue-dependent process that starts in liver and proceeds in WAT and is paralleled by tissue-specific gene expression changes, metabolic adjustments, changes in lipid composition, and inflammatory responses in Liver and WAT involving p65-NFkB and SOCS3. Expand
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