A5060349275- Endoplasmic Reticulum Stress and Disease
- Renal Diseases and Glomerulopathies
- Phagocytosis and Immune Regulation
- Autophagy in Disease and Therapy
- Dialysis and Renal Disease Management
- Social Media and Politics
- Genetic and Kidney Cyst Diseases
- Renal cell carcinoma treatment
- Biochemical Acid Research Studies
- Renal and related cancers
- Asian Culture and Media Studies
- Asian Industrial and Economic Development
- Biomedical Research and Pathophysiology
- Kidney Stones and Urolithiasis Treatments
- Mitochondrial Function and Pathology
- Advanced Glycation End Products research
- Pancreatic function and diabetes
- Redox biology and oxidative stress
- Forest Insect Ecology and Management
- Electoral Systems and Political Participation
- Chronic Kidney Disease and Diabetes
- Political Influence and Corporate Strategies
- Angiogenesis and VEGF in Cancer
- Urinary Bladder and Prostate Research
- Lysosomal Storage Disorders Research
Washington University in St. Louis
2016-2023
Kyung Hee University
2018
Abstract Misfolded protein aggregates may cause toxic proteinopathy, including autosomal dominant tubulointerstitial kidney disease due to uromodulin mutations (ADTKD- UMOD ), a leading hereditary disease. There are no targeted therapies. In our generated mouse model recapitulating human ADTKD- carrying mutation, we show that autophagy/mitophagy and mitochondrial biogenesis impaired, cGAS-STING activation tubular injury. Moreover, demonstrate inducible overexpression of mesencephalic...
Endoplasmic reticulum (ER) stress and disrupted proteostasis contribute to the pathogenesis of a variety glomerular tubular diseases. Thus, it is imperative develop noninvasive biomarkers for detecting ER in podocytes or cells incipient stage disease, when kidney biopsy not yet clinically indicated. Mesencephalic astrocyte–derived neurotrophic factor (MANF) localizes lumen secreted response several cell types. Here, using mouse models human nephrotic syndrome caused by mutant laminin β 2...
Significance Podocyte injury is the hallmark of nephrotic syndrome (NS), a leading cause chronic kidney disease affecting approximately 500 million people. We demonstrate that podocyte endoplasmic reticulum (ER) calcium release channel, type 2 ryanodine receptor (RyR2), undergoes phosphorylation during ER stress. The accelerated efflux due to leaky RyR2 activates cytosolic protease calpain 2, injury. Most importantly, we have identified chemical compound, K201, and biotherapeutic protein,...
Albuminuria is a hallmark of glomerular disease various etiologies. It not only symptom but also cause leading to glomerulosclerosis, interstitial fibrosis, and eventually, decline in kidney function. The molecular mechanism underlying albuminuria-induced injury remains poorly defined. In our genetic model nephrotic syndrome (NS), we have identified CHOP (C/EBP homologous protein)-TXNIP (thioredoxin-interacting protein) as critical linkers between ER dysfunction mitochondria dyshomeostasis....
DLG1 (discs-large homolog 1) and CASK (calcium/calmodulin-dependent serine protein kinase) interact at membrane-cytoskeleton interfaces function as scaffolding proteins that link signaling molecules, receptors, other intercellular synaptic junctions. Dlg1-null mice exhibit hydronephrosis, hydroureter, occasionally hypoplastic kidneys, whereas Cask-null do not. To investigate whether cooperate in the developing urogenital system, we generated deficient both either globally, 2) metanephric...
ER stress has emerged as a signaling platform underlying the pathogenesis of various kidney diseases. Thus, there is an urgent need to develop biomarkers in incipient stages stress–mediated disease, when biopsy not yet clinically indicated, for early therapeutic intervention. Cysteine-rich with EGF-like domains 2 (CRELD2) newly identified protein that induced and secreted under stress. For first time our knowledge, we demonstrate CRELD2 can serve sensitive urinary biomarker detecting...
Emerging evidence has highlighted the pivotal role of microvasculature injury in development and progression renal fibrosis. Angiopoietin-1 (Ang-1) is a secreted vascular growth factor that binds to endothelial-specific Tie2 receptor. Ang-1/Tie2 signaling critical for regulating blood vessel modulating response after injury, but dispensable mature, quiescent vessels. Although dysregulation endothelial (VEGF) been well studied pathologies, much less known about pathway interstitial Previous...
Autosomal dominant tubulointerstitial kidney disease (ADTKD)-uromodulin (
Misfolded protein aggregates may cause toxic proteinopathy, including autosomal dominant tubulointerstitial kidney disease due to uromodulin mutations (ADTKD- UMOD ), one of the leading hereditary diseases, and Alzheimer’s etc. There are no targeted therapies. ADTKD is also a genetic form renal fibrosis chronic disease, which affects 500 million people worldwide. For first time, in our newly generated mouse model recapitulating human ADTKD- carrying deletion mutation, we show that...