Publications by authors named "D Atzler"

Cardiovascular disease is the most common cause of mortality globally, accounting for approximately one out of three deaths. The main underlying pathology is atherosclerosis, a dyslipidemia-driven, chronic inflammatory disease. The interplay between immune cells and non-immune cells is of great importance in the complex process of atherogenesis.

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  • CCL17, produced by conventional dendritic cells, negatively affects regulatory T cells (Tregs) and contributes to atherosclerosis by suppressing Treg functions, but the exact mechanisms are still unclear.
  • Research on CCL17-deficient mice shows a different immune response that doesn't occur in mice lacking the CCR4 receptor, revealing a potential alternate signaling pathway involving CCR8 and CCL3.
  • The study finds that levels of CCL3 are linked to Treg activity and atherosclerosis severity, with increased CCL3 associated with disease progression, indicating a complex interaction that may impact therapeutic strategies.
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  • CD40L-CD40-TRAF signaling is implicated in the progression of atherosclerosis and the pathogenesis of coronary heart disease (CHD), especially in individuals with comorbid conditions like hyperlipidemia, diabetes, and hypertension.
  • In mouse models with diabetes and hypertension, treatment with a TRAF6 inhibitor showed promising results by normalizing oxidative stress and inflammation markers, suggesting that this signaling pathway could serve as a therapeutic target.
  • Analysis of plasma and vascular materials from CHD patients revealed a correlation between elevated inflammatory markers and comorbidities, indicating that addressing these inflammatory pathways could help reduce cardiovascular events in affected individuals.
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  • Atherosclerosis is an inflammatory disease primarily driven by lipids, and T cells are found to be the major immune cells involved in atherosclerotic plaques, highlighting the role of CBL-B in T cell activation.
  • Research on mice lacking the CBL-B protein showed smaller atherosclerotic lesions but increased T cell presence in the plaques, suggesting a complex relationship between T cells and atherosclerosis development.
  • The findings indicate that CBL-B regulates T cell activation and may influence overall inflammation in atherosclerosis, presenting it as a potential target for therapeutic intervention.
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Homoarginine (hArg) is a non-essential cationic amino acid which inhibits hepatic alkaline phosphatases to exert inhibitory effects on bile secretion by targeting intrahepatic biliary epithelium. We analyzed (1) the relationship between hArg and liver biomarkers in two large population-based studies and (2) the impact of hArg supplementation on liver biomarkers. We assessed the relationship between alanine transaminase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), alkaline phosphatases (AP), albumin, total bilirubin, cholinesterase, Quick's value, liver fat, and Model for End-stage Liver Disease (MELD) and hArg in appropriately adjusted linear regression models.

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