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Indoxyl sulphate‐initiated activation of cardiac fibroblasts is modulated by aryl hydrocarbon receptor and nuclear factor‐erythroid‐2‐related factor 2
1 INTRODUCTION Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) are at 5–10 fold higher the risk of cardiovascular disease (CVD) and cardiovascular (CV) events than age-matched controls.
Moderate Increase of Indoxyl Sulfate Promotes Monocyte Transition into Profibrotic Macrophages
The uremic toxin Indoxyl-3-sulphate (IS), a ligand of Aryl hydrocarbon Receptor (AhR), raises in blood during early renal dysfunction as a consequence of tubular damage, which may be present even when eGFR is normal or only moderately reduced, and promotes cardiovascular damage and monocyte-macrophage activation.
Testosterone Antagonizes Doxorubicin‐Induced Senescence of Cardiomyocytes
Background Chronic cardiotoxicity is less common in male than in female patients receiving doxorubicin and other anthracyclines at puberty and adolescence. We hypothesized that this sex difference might be secondary to distinct activities of sex hormones on cardiomyocyte senescence, which is thought to be central to the development of long‐term anthracycline cardiomyopathy.
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