A5031014098- Acute Kidney Injury Research
- Cardiac Ischemia and Reperfusion
- Anesthesia and Neurotoxicity Research
- Renal Diseases and Glomerulopathies
- Metabolism and Genetic Disorders
- Mass Spectrometry Techniques and Applications
- Metabolomics and Mass Spectrometry Studies
- Synthesis and Characterization of Heterocyclic Compounds
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- Chemotherapy-induced organ toxicity mitigation
- Sirtuins and Resveratrol in Medicine
- Immune Response and Inflammation
- Renal and related cancers
- Biomedical Research and Pathophysiology
- Macrophage Migration Inhibitory Factor
- Bipolar Disorder and Treatment
- FOXO transcription factor regulation
- Nuclear Receptors and Signaling
- Genetic and Kidney Cyst Diseases
- Drug-Induced Hepatotoxicity and Protection
- Adipose Tissue and Metabolism
- Metabolism, Diabetes, and Cancer
- Analytical Chemistry and Chromatography
- Phagocytosis and Immune Regulation
National Institute of Environmental Health Sciences
2023-2024
National Institutes of Health
2023-2024
Medical University of South Carolina
2014-2019
University of Arizona
2017-2018
Ralph H. Johnson VA Medical Center
2014
Although disruption of mitochondrial homeostasis and biogenesis (MB) is a widely accepted pathophysiologic feature sepsis-induced acute kidney injury (AKI), the molecular mechanisms responsible for this phenomenon are unknown. In study, we examined signaling pathways suppression MB in mouse model lipopolysaccharide (LPS)-induced AKI. Downregulation peroxisome proliferator-activated receptor <i>γ</i> coactivator-1<i>α</i> (PGC-1<i>α</i>), master regulator MB, was noted at mRNA level 3 hours...
The upregulation of kidney injury molecule-1 (KIM-1) has been extensively studied in various renal diseases and following acute injury; however, the initial mechanisms controlling KIM-1 expression remain limited. In this study, was examined mouse cell cultures two different models (AKI), ischemia reperfusion (IR)–induced lipopolysaccharide (LPS)-induced sepsis. mRNA increased both AKI models, pharmacological inhibition extracellular signal–regulated kinase 1/2 (ERK1/2) signaling attenuated...
Our laboratory previously reported that agonists of the 5-hydoxytryptamine 1F (5-HT
Deficiency in the transcription factor (TF) GLI-Similar 3 (GLIS3) humans and mice leads to development of polycystic kidney disease (PKD). In this study, we investigate role GLIS3 regulation energy metabolism mitochondrial functions relation its normal metabolic reprogramming PKD pathogenesis.
Feature finding is a common way to process untargeted mass spectrometry (MS) data obtain list of chemicals present in sample. Most feature algorithms naïvely search for patterns unique descriptors (e.g., m/z, retention time, and mobility) provide unannotated features. There need solutions processing MS data, independent chemical or origin, assess features based on measurement quality with the aim improving interpretation. Here, we report signal response evaluation as method by which...
Background We previously demonstrated that extracellular signal‐regulated kinase 1/2 (ERK1/2) is activated rapidly following renal ischemia‐reperfusion injury (IRI) and downregulates PGC‐1α, a transcriptional coactivator involved in the regulation of cellular mitochondrial metabolism. Recently, PGC‐1α has been implicated regulating nicotinamide adenine dinucleotide (NAD + ) biosynthesis leading to better outcomes acute kidney (AKI). NAD vital coenzyme for energy metabolism, redox signaling,...
Background Because substantial damage can occur before detection of acute kidney injury (AKI) new early predictor biomarkers are needed, such as molecule‐1 (KIM‐1). KIM‐1 is a transmembrane glycoprotein that expressed at very low levels in healthy and highly upregulated during injury. shed be detected blood urine. While has been studied various models AKI, the regulatory mechanisms leading to upregulation remains limited. Here, we explored role ERK1/2 activation on expression following...