A5055227001- Acute Kidney Injury Research
- Renin-Angiotensin System Studies
- Nitric Oxide and Endothelin Effects
- Inflammatory mediators and NSAID effects
- Synthesis and bioactivity of alkaloids
- Drug-Induced Hepatotoxicity and Protection
- Chronic Kidney Disease and Diabetes
- Atherosclerosis and Cardiovascular Diseases
- Dialysis and Renal Disease Management
- Coenzyme Q10 studies and effects
- Heme Oxygenase-1 and Carbon Monoxide
- Apelin-related biomedical research
- Pharmacogenetics and Drug Metabolism
- Diverse Scientific Research Studies
- Biochemical Acid Research Studies
- Hormonal Regulation and Hypertension
- Polyamine Metabolism and Applications
- Metabolomics and Mass Spectrometry Studies
- Cannabis and Cannabinoid Research
- Neonatal Health and Biochemistry
- Bioactive Compounds and Antitumor Agents
- Erythrocyte Function and Pathophysiology
- Cancer therapeutics and mechanisms
- Amino Acid Enzymes and Metabolism
Humboldt-Universität zu Berlin
2020-2024
Charité - Universitätsmedizin Berlin
2020-2024
Freie Universität Berlin
2020-2024
RELX Group (United States)
2023
University of Vienna
2020
Kiel University
2020
BACKGROUND: Acute hyperglycemia is a risk factor for developing acute kidney injury and poor renal outcome in critically ill patients, whereby the role of vasculature remains unclear. We hypothesize that hyperglycemia-associated hyperosmolarity facilitates vasodilation through Piezo1-mediated eNOS (endothelial NO synthase) activation. METHODS: Vasoreactivity was analyzed using wire myography isolated mouse mesenteric arteries interlobar, microvascular perfusion afferent arterioles efferent...
The benzo[c]phenanthridine P8-D6 was recently found to suppress the catalytic activity of both human topoisomerase (Topo) I and II. Concomitantly, potent cytotoxic observed in different tumor cell lines, raising questions about underlying mechanisms vitro. In present study, we addressed question whether acts as a so-called Topo poison, stabilizing covalent Topo–DNA intermediate, thus inducing fatal DNA strand breaks proliferating cells. HT-29 colon carcinoma cells, fluorescence imaging...
Renal arteriolar tone depends considerably on the dilatory action of nitric oxide (NO) via activation soluble guanylyl cyclase (sGC) and cGMP action. NO deficiency hypoxia/reoxygenation are important pathophysiological factors in development acute kidney injury. It was hypothesized that NO-sGC-cGMP system functions differently renal afferent arterioles (AA) compared with efferent (EA) sGC activator cinaciguat differentially dilates these arterioles. Experiments were performed isolated,...
Endothelial dysfunction (ED) comes with age, even without overt vessel damage such as that which occurs in atherosclerosis and diabetic vasculopathy. We hypothesized aging would affect the downstream signalling of endothelial nitric oxide (NO) system vascular smooth muscle (VSM). With this mind, resistance mesenteric arteries were isolated from 13-week (juvenile) 40-week-old (aged) mice tested under isometric conditions using wire myography. Acetylcholine (ACh)-induced relaxation was reduced...
Reduced renal medullary oxygen supply is a key factor in the pathogenesis of acute kidney injury (AKI). As medulla exclusively receives blood through descending vasa recta (DVR), dilating these microvessels after AKI may help renoprotection by restoring flow. We stimulated NO-sGC-cGMP signalling pathway DVR at three different levels before and hypoxia/re-oxygenation (H/R). Rat were isolated perfused under isobaric conditions. The phosphodiesterase 5 (PDE5) inhibitor sildenafil (10-6 mol/L)...
PubMed search of the keywords “acute kidney injury (AKI)” or “chronic disease (CKD)” shows doubling number hits in last decade when compared to all years before. Even taking a certain “inflation” scientific publication into account, this observation reflects enormous interest these syndromes. In fact, incidence AKI is increasing population general hospitalized patients.1 Furthermore, in-hospital mortality high patients, which emphasizes need for an effective treatment.2 and CKD are closely...
<p class="first" dir="auto" id="d1473669e141">After an acute kidney injury (AKI), patients face elevated morbidity and mortality rates, often progressing to chronic disease (CKD). Restoring adequate blood supply can prevent renal tissue hypoxia nephron loss. Soluble guanylate cyclase (sGC) serves as a promising target for vasodilation mediation. Our study aims explore whether pharmacological sGC activation enhance perfusion, thus mitigating hypoxic damage post-AKI....