David A. Brenner

ORCID: 0000-0003-2573-525X
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About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Liver physiology and pathology
  • Liver Disease and Transplantation
  • NF-κB Signaling Pathways
  • Alcohol Consumption and Health Effects
  • Organ Transplantation Techniques and Outcomes
  • Liver Diseases and Immunity
  • Endoplasmic Reticulum Stress and Disease
  • Immune Response and Inflammation
  • Cell death mechanisms and regulation
  • Diet, Metabolism, and Disease
  • Pancreatic function and diabetes
  • Drug-Induced Hepatotoxicity and Protection
  • Hepatitis B Virus Studies
  • Pediatric Hepatobiliary Diseases and Treatments
  • Gut microbiota and health
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Porphyrin Metabolism and Disorders
  • Digestive system and related health
  • Pancreatitis Pathology and Treatment
  • TGF-β signaling in diseases
  • Cell Adhesion Molecules Research
  • Diet and metabolism studies
  • Clinical Nutrition and Gastroenterology
  • RNA Interference and Gene Delivery

Universität Ulm
2015-2025

Discovery Institute
2022-2025

Sanford Burnham Prebys Medical Discovery Institute
2022-2025

University of California, San Diego
2015-2024

Masaryk University
2024

UC San Diego Health System
2009-2022

University of California San Diego Medical Center
1988-2021

University of Southern California
1998-2020

Southern California Reproductive Center
2011-2020

La Jolla Alcohol Research
2019

Myofibroblasts produce the fibrous scar in hepatic fibrosis. In carbon tetrachloride (CCl(4)) model of liver fibrosis, quiescent stellate cells (HSC) are activated to become myofibroblasts. When underlying etiological agent is removed, clinical and experimental fibrosis undergoes a remarkable regression with complete disappearance these Although some myofibroblasts apoptose, it unknown whether other may revert an inactive phenotype during We elucidated fate HSCs/myofibroblasts recovery from...

10.1073/pnas.1201840109 article EN Proceedings of the National Academy of Sciences 2012-05-07

The translocation of bacteria and bacterial products into the circulation contributes to alcoholic liver disease. Intestinal overgrowth is common in patients with aims our study were investigate translocation, changes enteric microbiome, its regulation by mucosal antimicrobial proteins We used a mouse model continuous intragastric feeding alcohol or an isocaloric diet. Bacterial occurred prior observed microbiome. Quantitative intestinal microflora these animals assessed first using...

10.1002/hep.24018 article EN Hepatology 2010-09-30

Abstract NF-κB plays a critical role in the transcriptional regulation of proinflammatory gene expression various cells. Cytokine-mediated activation requires kinases, which ultimately leads to phosphorylation and degradation IκB, cytoplasmic inhibitor. The food derivative curcumin has been shown inhibit activity some cell types. In this report we investigate mechanism action on cytokine-induced using intestinal epithelial cells (IEC). Curcumin inhibited IL-1β-mediated ICAM-1 IL-8 IEC-6,...

10.4049/jimmunol.163.6.3474 article EN The Journal of Immunology 1999-09-15

Bacterial lipopolysaccharide (LPS) stimulates Kupffer cells and participates in the pathogenesis of alcohol–induced liver injury. However, it is unknown whether LPS directly affects hepatic stellate (HSCs), main fibrogenic cell type injured liver. This study characterizes LPS–induced signal transduction proinflammatory gene expression activated human HSCs. Culture–activated HSCs isolated from patients with hepatitis C virus–induced cirrhosis express LPS–associated signaling molecules,...

10.1053/jhep.2003.50182 article EN Hepatology 2003-05-01

Activation and accumulation of cardiac fibroblasts, which result in excessive extracellular matrix deposition consequent mechanical stiffness, myocyte uncoupling, ischemia, are key contributors to heart failure progression. Recently, endothelial-to-mesenchymal transition (EndoMT) the recruitment circulating hematopoietic progenitors have been reported generate substantial numbers fibroblasts response pressure overload–induced injury; therefore, these processes widely considered be promising...

10.1172/jci74783 article EN Journal of Clinical Investigation 2014-06-17

Angiotensin II (Ang II) is a pro-oxidant and fibrogenic cytokine. We investigated the role of NADPH oxidase in Ang II–induced effects hepatic stellate cells (HSCs), cell type. Human HSCs express mRNAs key components nonphagocytic oxidase. phosphorylated p47phox, regulatory subunit oxidase, induced reactive oxygen species formation via activity. AKT MAPKs increased AP-1 DNA binding redox-sensitive manner. stimulated synthesis, migration, procollagen α1(I) mRNA expression, secretion TGF-β1...

10.1172/jci18212 article EN Journal of Clinical Investigation 2003-11-01

The magnetic resonance imaging-estimated proton density fat fraction (MRI-PDFF) is a novel imaging-based biomarker that allows mapping of the entire liver, whereas spectroscopy-measured (MRS-PDFF) provides biochemical measure liver in small regions interest. Cross-sectional studies have shown MRI-PDFF correlates with MRS-PDFF. aim this study was to show utility assessing quantitative changes through three-way comparison and MRS-PDFF histology-determined steatosis grade at two time points...

10.1002/hep.26455 article EN Hepatology 2013-05-20
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