A5003974636- Redox biology and oxidative stress
- Clinical Nutrition and Gastroenterology
- Ferroptosis and cancer prognosis
- Mitochondrial Function and Pathology
- Inflammatory mediators and NSAID effects
- Alzheimer's disease research and treatments
- Adipose Tissue and Metabolism
- Muscle Physiology and Disorders
- Exercise and Physiological Responses
- Fatty Acid Research and Health
- Tryptophan and brain disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Bone health and osteoporosis research
- Genomics, phytochemicals, and oxidative stress
- Inflammatory Bowel Disease
- Genetics, Aging, and Longevity in Model Organisms
- Selenium in Biological Systems
- Epigenetics and DNA Methylation
- Heat shock proteins research
- Cancer, Lipids, and Metabolism
- Connective tissue disorders research
- Digestive system and related health
- RNA modifications and cancer
- ATP Synthase and ATPases Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
The University of Texas Health Science Center at San Antonio
2016-2025
South Texas Veterans Health Care System
2013-2024
The University of Texas Health Science Center at Houston
2007-2022
Institute for Neurodegenerative Disorders
2022
The University of Texas at San Antonio
2018
Audie L. Murphy Memorial VA Hospital
2013-2015
Geriatric Research Education and Clinical Center
2006-2013
Texas A&M University
2011
College Station Medical Center
2011
Nagoya University
2011
Synaptic loss and neuron death are the underlying cause of neurodegenerative diseases such as Alzheimer's disease (AD); however, modalities cell in those remain unclear. Ferroptosis, a newly identified oxidative mechanism triggered by massive lipid peroxidation, is implicated degeneration neurons populations spinal motor midbrain neurons. Here, we investigated whether forebrain regions (cerebral cortex hippocampus) that severely afflicted AD patients might be vulnerable to ferroptosis. To...
Abstract The increased incidence of inflammatory bowel disease (IBD) has become a global phenomenon that could be related to adoption Western life-style. Westernization dietary habits is partly characterized by enrichment with the ω-6 polyunsaturated fatty acid (PUFA) arachidonic (AA), which entails risk for developing IBD. Glutathione peroxidase 4 (GPX4) protects against lipid peroxidation (LPO) and cell death termed ferroptosis. We report small intestinal epithelial cells (IECs) in Crohn’s...
Glutathione peroxidase 4 (Gpx4) is uniquely involved in the detoxification of oxidative damage to membrane lipids. Our previous studies showed that Gpx4 essential for mouse survival and deficiency makes cells vulnerable injury. In present study, we generated two lines transgenic mice overexpressing (Tg(GPX4) mice) using a genomic clone containing human GPX4 gene. Both Tg-(GPX4) mice, Tg5 Tg6, had elevated levels (mRNA protein) all tissues investigated, overexpression did not cause...
This study aimed to determine whether aging negatively affects MSC replication and osteogen-esis these features could be altered by exposure an extracellular matrix (ECM) generated marrow cells from young or old mice. A cell-free ECM was prepared cultured femoral either 3- 18-mo-old C57BL/6 mice (young-ECM old-ECM, respectively). The osteo-genesis of MSCs maintained on young-ECM vs. old-ECM as well plastic were examined in vitro vivo. We found that the frequency mice, measured colony-forming...
Glutathione peroxidase 4 (Gpx4) is an essential antioxidant enzyme having multiple functions. A long form Gpx4 protein and a short protein, which are distinguishable by the presence or lack of mitochondrial signal peptide at N terminus, generated from gene. In this study, we transgenic mice using mutated GPX4 genes encoding either (lGPX4 gene) (sGPX4 gene). Our results showed that with sGPX4 gene had increased in all tissues were protected against diquat-induced apoptosis liver. Moreover,...
Summary H 2 O is a major reactive oxygen species produced by mitochondria that implicated to be important in aging and pathogenesis of diseases such as diabetes; however, the cellular physiological roles mitochondrial remain poorly understood. Peroxiredoxin 3 (Prdx3/Prx3) thioredoxin peroxidase localized mitochondria. To understand age‐associated diseases, we generated transgenic mice overexpressing Prdx3 (Tg(PRDX3) mice). Tg(PRDX3) overexpress broad range tissues, overexpression occurs...
Abstract Degeneration and death of motor neurons in Amyotrophic Lateral Sclerosis (ALS) are associated with increased lipid peroxidation. Lipid peroxidation is the driver ferroptosis, an iron-dependent oxidative mode cell death. However, importance ferroptosis neuron degeneration ALS remains unclear. Glutathione peroxidase 4 (Gpx4) a key enzyme suppressing by reducing phospholipid hydroperoxides membranes. To assess effect protection against on disease, we generated SOD1 G93A GPX4 double...
Background & AimsCrohn's disease (CD) globally emerges with Westernization of lifestyle and nutritional habits. However, a specific dietary constituent that comprehensively evokes gut inflammation in human inflammatory bowel diseases remains elusive. We aimed to delineate how increased intake polyunsaturated fatty acids (PUFAs) Western diet, known impart risk for developing CD, affects course. hypothesized the unfolded protein response antioxidative activity glutathione peroxidase 4 (GPX4),...
Axonal fusion represents an efficient way to recover function after nerve injury. However, how axonal is induced and regulated remains largely unknown. We discover that ferroptosis signaling can promote functional recovery in C. elegans a dose-sensitive manner. Ferroptosis-induced lipid peroxidation enhances injury-triggered phosphatidylserine exposure (PS) through PS receptor (PSR-1) EFF-1 fusogen. Axon injury induces PSR-1 condensate formation disruption of condensation inhibits fusion....
Increased lipid peroxidation is shown to be an early event of Alzheimer's disease (AD). However, it not clear whether and how increased might lead amyloidogenesis, a hallmark AD. Glutathione peroxidase 4 (Gpx4) essential antioxidant defense enzyme that protects organism against peroxidation. Gpx4+/- mice show in brain, as evidenced by their elevated levels 4-hydroxy-2-nonenal. To understand the role we studied secretase activities function age. Both young (6 months) middle-aged (17-20 had...
Abstract Age‐related muscle atrophy and weakness, or sarcopenia, are significant contributors to compromised health quality of life in the elderly. While mechanisms driving this pathology not fully defined, reactive oxygen species, neuromuscular junction (NMJ) disruption, loss innervation important risk factors. The goal study is determine impact mitochondrial hydrogen peroxide on neurogenic contractile dysfunction. Mice with muscle‐specific overexpression H 2 O scavenger peroxiredoxin3...
Reactive oxygen species (ROS) accumulation is a cardinal feature of skeletal muscle atrophy. ROS refers to collection radical molecules whose cellular signals are vast, and it unclear which downstream consequences responsible for the loss mass strength. Here, we show that lipid hydroperoxides (LOOH) increased with age disuse, LOOH by deletion glutathione peroxidase 4 (GPx4) sufficient augment promoted atrophy in lysosomal-dependent, proteasomal-independent manner. In young old mice, genetic...
Abstract Polyunsaturated fatty acids (PUFA) in membrane lipids are prone to attack by reactive oxygen species (ROS), and the resulting lipid peroxidation can cause injury death of cells. Glutathione peroxidase 4 (Gpx4) is an antioxidant defense enzyme that directly detoxify hydroperoxides generated ROS. Overexpression Gpx4 has been shown be protective against oxidative damage several cell lines. We examined this study stress response neurons with increased expression Gpx4, because especially...