A5045038056- Chronic Kidney Disease and Diabetes
- Acute Kidney Injury Research
- Cell death mechanisms and regulation
- Renal Diseases and Glomerulopathies
- NF-κB Signaling Pathways
- Phagocytosis and Immune Regulation
- Dialysis and Renal Disease Management
- Renal and related cancers
- Nuclear Receptors and Signaling
- Parathyroid Disorders and Treatments
- Inflammasome and immune disorders
- Trace Elements in Health
- Biomedical Research and Pathophysiology
- Genetic and Kidney Cyst Diseases
- Immune Response and Inflammation
- Endoplasmic Reticulum Stress and Disease
- Macrophage Migration Inhibitory Factor
- Vitamin C and Antioxidants Research
- Drug-Induced Hepatotoxicity and Protection
- Pancreatitis Pathology and Treatment
- Heme Oxygenase-1 and Carbon Monoxide
- Muscle and Compartmental Disorders
- Advanced Glycation End Products research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Epigenetics and DNA Methylation
Universidad Autónoma de Madrid
2015-2024
Hospital Universitario Fundación Jiménez Díaz
2015-2024
Universidad Complutense de Madrid
2003-2024
Fundación Renal
2011-2024
Instituto de Salud Carlos III
2008-2024
RELX Group (United States)
2022-2023
Spanish Clinical Research Network
2014-2022
Universidad de Alcalá
1993-2022
Centre de Recherche des Cordeliers
2016
Inserm
2016
Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there one common pathway in which CypD RIPK1 act or separate RN pathways exist. Here, we demonstrate that necroptosis ischemia-reperfusion injury (IRI) mice occurs as primary organ damage, independent of the immune system, deficient for RIPK3, essential downstream partner are...
AKI is histologically characterized by necrotic cell death and inflammation. Diverse pathways of regulated necrosis have been reported to contribute AKI, but the molecular regulators involved remain unclear. We explored relative contributions ferroptosis necroptosis folic acid (FA)-induced in mice. FA-AKI mice associates with lipid peroxidation downregulation glutathione metabolism proteins, features that are typical ferroptotic death. show ferrostatin-1 (Fer-1), an inhibitor ferroptosis,...
Proinflammatory cytokines contribute to renal injury, but the downstream effectors within kidney cells are not well understood. One candidate effector is Klotho, a protein expressed by that has antiaging properties; Klotho-deficient mice have an accelerated aging-like phenotype, including vascular injury and injury. Whether proinflammatory cytokines, such as TNF TNF-like weak inducer of apoptosis (TWEAK), modulate Klotho unknown. In mice, exogenous administration TWEAK decreased expression...
Tenofovir is an acyclic nucleotide analogue reverse-transcriptase inhibitor structurally similar to the nephrotoxic drugs adefovir and cidofovir. widely used treat HIV infection approved for treatment of hepatitis B virus. Despite initial cell culture clinical trials results supporting renal safety tenofovir, its use associated with a low, albeit significant, risk kidney injury. Proximal tubular secretion tenofovir explains accumulation drug in these mitochondria-rich cells. nephrotoxicity...
Acute kidney injury is a common complication of rhabdomyolysis. A better understanding this syndrome may be useful to identify novel therapeutic targets because there no specific treatment so far. Ferroptosis an iron-dependent form regulated nonapoptotic cell death that involved in renal injury. In study, we investigated whether ferroptosis associated with rhabdomyolysis-mediated damage, and studied the effect curcumin, powerful antioxidant renoprotective properties. Induction rhabdomyolysis...
Background. Transforming growth factor-β1 (TGF-β1) and the macrophage inhibitory factor receptor CD74 link metabolic disorder with tissue injury in diabetic nephropathy. Fabry disease is an X-linked lysosomal glycosphingolipid storage resulting from a deficient activity of α-galactosidase A that leads to proteinuric renal injury. However, between abnormality poorly characterized. Globotriaosylsphingosine (lyso-Gb3) was recently identified as bioactive molecule accumulating disease. We...
TNF-like weak inducer of apoptosis (TWEAK) is a member the TNF superfamily cytokines. In addition to binding and activating fibroblast growth factor–inducible 14 receptor, TWEAK may regulate apoptosis, proliferation, inflammation; however, role this system in kidney injury unknown. vitro, it was found that induced sustained activation NF-κB murine tubular epithelial cell line (MCT). associated with degradation IκB-α; translocation RelA nucleus; increased mRNA protein expression monocyte...
Activation of Janus kinase/signal transducers and activators transcription (JAK/STAT) is an important mechanism by which hyperglycemia contributes to renal damage, suggesting that modulation this pathway may prevent vascular complications diabetes. Here, we investigated the involvement suppressors cytokine signaling (SOCS) as intracellular negative regulators JAK/STAT activation in diabetic nephropathy. In a rat model, inducing diabetes resulted increased expression SOCS1 SOCS3. humans,...
Acute kidney injury (AKI) is a potentially lethal condition for which no therapy available beyond replacement of renal function. Post-translational histone modifications modulate gene expression and injury. Histone crotonylation recently described post-translational modification. We hypothesized that might was studied in cultured murine proximal tubular cells kidneys from mice with AKI induced by folic acid or cisplatin. lysine observed healthy human tissue. Kidney tissue increased during...
Significance Acute kidney injury (AKI) has a mortality of 50%. There is no satisfactory therapy and the incidence increasing. The etiology AKI heterogeneous, this therapeutic implications. Here we show that necroptosis plays role in second wave tubular cell death experimental toxic AKI. This triggered by TWEAK activation Fn14 receptor contributes to persistence injury. We previously observed initial was ferroptosis dependent independent. identification pathway contributing may facilitate...
Podocyte injury is an early feature of Fabry nephropathy, but the molecular mechanisms podocyte are poorly understood. Lyso-Gb3 accumulates in serum disease and increases extracellular matrix synthesis podocytes. We explored contribution Notch1 signaling, a mediator injury, to lyso-Gb3-elicited responses cultured human At clinically relevant concentrations, lyso-Gb3 activates resulting increased active HES1, canonical Notch transcriptional target. A γ-secretase inhibitor or specific small...