Publications by authors named "F Eitner"

Article Synopsis
  • - Chronic kidney disease (CKD) progression is linked to oxidative stress damaging the NO-sGC-cGMP signaling pathway, but runcaciguat is a new drug that can activate dysfunctional sGC and restore this signaling under such conditions.
  • - In studies with ZSF1 rats (a model for CKD/DKD), runcaciguat significantly reduced proteinuria and improved kidney function compared to placebo over a 12-week period with varying doses.
  • - The treatment also positively impacted metabolic markers, reducing high blood sugar levels (HbA1c), triglycerides, and cholesterol in obese ZSF1 rats, suggesting its potential as a kidney-protective treatment.
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Diabetic kidney disease (DKD) is the most common cause of renal failure. Therapeutics development is hampered by our incomplete understanding of animal models on a cellular level. We show that ZSF1 rats recapitulate human DKD on a phenotypic and transcriptomic level.

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Despite advances in the treatment of heart failure in recent years, options for patients are still limited and the disease is associated with considerable morbidity and mortality. Modulating cyclic guanosine monophosphate levels within the natriuretic peptide signaling pathway by inhibiting PDE9A has been associated with beneficial effects in preclinical heart failure models. We herein report the identification of BAY-7081, a potent, selective, and orally bioavailable PDE9A inhibitor with very good aqueous solubility starting from a high-throughput screening hit.

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Article Synopsis
  • Immunoglobulin A (IgA) plays a crucial role in immune response to food and pathogens and is linked to various conditions like celiac disease and inflammatory bowel disease.
  • A genome-wide association study examined blood IgA levels in over 41,000 people, identifying 20 key genetic loci that affect IgA levels, including novel genes.
  • Findings suggest genetic factors influencing IgA can impact diseases such as IgA nephropathy and type 2 diabetes, with African ancestry showing higher IgA levels and more IgA-increasing genetic variants.
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