A5015868168- Renal Diseases and Glomerulopathies
- Complement system in diseases
- Vasculitis and related conditions
- Chronic Kidney Disease and Diabetes
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- COVID-19 Clinical Research Studies
- T-cell and B-cell Immunology
- Systemic Lupus Erythematosus Research
- Autoimmune Bullous Skin Diseases
- Genetic and Kidney Cyst Diseases
- Platelet Disorders and Treatments
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Renal and related cancers
- Single-cell and spatial transcriptomics
- Tuberous Sclerosis Complex Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Renin-Angiotensin System Studies
- Renal Transplantation Outcomes and Treatments
- Pituitary Gland Disorders and Treatments
- Biomedical Research and Pathophysiology
- Cancer, Hypoxia, and Metabolism
- Adrenal and Paraganglionic Tumors
- Otitis Media and Relapsing Polychondritis
- Genomic variations and chromosomal abnormalities
- Long-Term Effects of COVID-19
Universität Hamburg
2016-2025
University Medical Center Hamburg-Eppendorf
2016-2025
University Hospital Heidelberg
2016-2024
Johns Hopkins University
2024
University Medical Center
2023-2024
Sorbonne Université
2024
Aarhus University
2024
Heidelberg University
2016-2024
Arkana Laboratories
2018-2024
Inserm
2024
Injury and loss of podocytes are leading factors glomerular disease renal failure. The postmitotic podocyte is the primary target for toxic, immune, metabolic, oxidant stress, but little known about how this cell type copes with stress. Recently, autophagy has been identified as a major pathway that delivers damaged proteins organelles to lysosomes in order maintain cellular homeostasis. Here we report exhibit an unusually high level constitutive autophagy. Podocyte-specific deletion...
Chronic glomerular diseases, associated with renal failure and cardiovascular morbidity, represent a major health issue. However, they remain poorly understood. Here we have reported that tightly controlled mTOR activity was crucial to maintaining podocyte function, while dysregulation of facilitated diseases. Genetic deletion complex 1 (mTORC1) in mouse podocytes induced proteinuria progressive glomerulosclerosis. Furthermore, simultaneous both mTORC1 mTORC2 from aggravated the lesions,...
Autophagy is responsible for the degradation of protein aggregates and damaged organelles. Several studies have reported increased autophagic activity in tubular cells after kidney injury. Here, we examine role cell autophagy vivo under both physiological conditions stress using two different tubular-specific Atg5-knockout mouse models. While Atg5 deletion distal tubule does not cause a significant alteration function, deleting proximal results impaired function. Already conditions,...
Thrombospondin type 1 domain–containing 7A (THSD7A) is a target antigen identified in adult membranous nephropathy (MN) along with the major phospholipase A 2 receptor (PLA R1). The prevalence of THSD7A-Ab–positive patients unknown, and it unclear whether clinical presentation differs between positive for PLA R1-Ab or THSD7A-Ab. We screened serum samples 1276 MN from three different cohorts presence THSD7A-Ab by Western blot analysis newly developed indirect immunofluorescence test (IFT)....
Th17 cells are most abundant in the gut, where their presence depends on intestinal microbiota. Here, we examined whether contribute to extra-intestinal responses autoimmune kidney disease. We found high frequencies of kidneys patients with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis. utilized photoconversion Kaede mice track T cell mobilization upon glomerulonephritis induction, and that egress from gut a S1P-receptor-1-dependent fashion subsequently migrate...
Minimal change disease and primary focal segmental glomerulosclerosis in adults, along with idiopathic nephrotic syndrome children, are immune-mediated podocytopathies that lead to syndrome. Autoantibodies targeting nephrin have been found patients minimal disease, but their clinical pathophysiological roles unclear.
Abstract Membranous nephropathy (MN) is an antibody-mediated autoimmune disease characterized by glomerular immune complexes containing complement components. However, both the initiation pathways and pathogenic significance of activation in MN are poorly understood. Here, we show that components from all three (alternative, classical lectin) found renal biopsies patients with MN. Proximity ligation assays to directly visualize assembly tissue reveal dominant via pathway, a close correlation...
Neutrophil trafficking to sites of inflammation is essential for the defense against bacterial and fungal infections, but also contributes tissue damage in TH17-mediated autoimmunity. This process regulated by chemokines, which often show an overlapping expression pattern function pathogen- autoimmune-induced inflammatory reactions. Using a murine model crescentic GN, we that pathogenic TH17/IL-17 immune response induces chemokine (C-X-C motif) ligand 5 (CXCL5) kidney tubular cells, recruits...
Although it is well established that microbial infections predispose to autoimmune diseases, the underlying mechanisms remain poorly understood. After infection, tissue-resident memory T (TRM) cells persist in peripheral organs and provide immune protection against reinfection. However, whether TRM participate responses unrelated primary such as inflammation, unknown. By using high-dimensional single-cell analysis, we identified CD4+ with a TH17 signature (termed TRM17 cells) kidneys of...
The cellular origins of glomerulosclerosis involve activation parietal epithelial cells (PECs) and progressive podocyte depletion. While mammalian target rapamycin-mediated (mTOR-mediated) hypertrophy is recognized as an important signaling pathway in the context glomerular disease, role a compensatory mechanism preventing PEC remains poorly understood. In this study, we show that mTOR activation-related genes were both upregulated intercorrelated biopsies from patients with focal segmental...
Primary membranous nephropathy (MN) is caused by circulating autoantibodies binding to antigens on the podocyte surface. PLA2R1 main target antigen in 70%-80% of cases, but pathogenesis unresolved 10%-15% patients.We used native western blotting identify IgG4 autoantibodies, which bind an endogenously expressed membranes, serum index patient with MN. These were immunoprecipitate antigen, and mass spectrometry was Netrin G1 (NTNG1). Using blot ELISA, NTNG1 analyzed cohorts 888 patients MN or...
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and histopathologic glomerular lesions are among earliest structural alterations DN. However, signaling pathways that initiate these incompletely understood.To delineate cellular molecular basis for DN initiation, we performed single-cell bulk RNA sequencing cells from type 2 diabetes mice (BTBR ob/ob) at early stage DN.Analysis differentially expressed genes revealed glucose-independent responses in cell types. The...
Myeloperoxidase (MPO)-specific antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (MPO-ANCA-associated vasculitis) is one of two major ANCA-associated variants characterised by systemic necrotising with few or no immune deposits. MPO-ANCA-associated predominantly affects small blood vessels and, in contrast to its counterpart proteinase 3-ANCA-associated vasculitis, generally not associated granulomatous inflammation. The kidneys and lungs are the most commonly affected organs....
Background. ABO-incompatible living donor kidney transplantation based on specific conditioning has been successfully adopted by transplant centres worldwide. Excellent short-term results have reported in small cohorts. However, long-term data and comparative analyses are still sparse. We report the outcome of 40 consecutive recipients compare their clinical course to a control group 43 ABO-compatible patients transplanted during same time period.
Tenofovir disoproxil fumarate (tenofovir DF) use has been associated with renal dysfunction and Fanconi syndrome. is taken up into tubules by anion transporters where high intracellular drug concentration may induce a functionally relevant depletion of mitochondrial DNA (mtDNA). We investigated if tenofovir mtDNA respiratory chain dysfunction.Rats (n = 8) were gavaged daily 100 mg x kg(-1) d(-1) DF or didanosine. Kidneys livers examined after 8 weeks treatment.The group had significantly...