A5004156315- Diet and metabolism studies
- Inflammasome and immune disorders
- Autophagy in Disease and Therapy
- Autism Spectrum Disorder Research
- Diet, Metabolism, and Disease
- Mesenchymal stem cell research
- Calcium signaling and nucleotide metabolism
- Cholesterol and Lipid Metabolism
- Epigenetics and DNA Methylation
- Atherosclerosis and Cardiovascular Diseases
- Cancer, Lipids, and Metabolism
- Endoplasmic Reticulum Stress and Disease
- Kruppel-like factors research
- Metabolism, Diabetes, and Cancer
- Muscle metabolism and nutrition
- Sphingolipid Metabolism and Signaling
- Biochemical Analysis and Sensing Techniques
- Ferroptosis and cancer prognosis
- Aortic aneurysm repair treatments
- Macrophage Migration Inhibitory Factor
- Nutrition, Genetics, and Disease
- Aortic Disease and Treatment Approaches
- Nutrition and Health in Aging
- Nutritional Studies and Diet
- Adipose Tissue and Metabolism
Washington University in St. Louis
2018-2024
The autophagy-lysosome system is an important cellular degradation pathway that recycles dysfunctional organelles and cytotoxic protein aggregates. A decline in this pathogenic many human diseases including neurodegenerative disorders, fatty liver disease, atherosclerosis. Thus there intense interest discovering therapeutics aimed at stimulating the system. Trehalose a natural disaccharide composed of two glucose molecules linked by ɑ-1,1-glycosidic bond with unique ability to induce...
Dysfunction in the macrophage lysosomal system including reduced acidity and diminished degradative capacity is a hallmark of atherosclerosis, leading to blunted clearance excess cellular debris lipids plaques contributing lesion progression. Devising strategies rescue this dysfunction novel therapeutic measure. Nanoparticles have emerged as an effective platform both target specific tissues serve drug delivery vehicles. In most cases, administered nanoparticles are taken up non-selectively...
The mTOR (mechanistic target of rapamycin) pathway is a complex signaling cascade that regulates cellular growth, proliferation, metabolism, and survival. Although activation has been linked to atherosclerosis, its direct role in lesion progression plaque macrophages remains poorly understood. We previously demonstrated mTORC1 (mTOR 1) promotes atherogenesis through inhibition autophagy increased apoptosis macrophages.
Galectin-3 (Gal3) is a β-galactoside-binding lectin predominantly known as secreted inflammatory biomarker in cardiovascular disease, with significantly elevated circulating levels patients atherosclerosis and myocardial infarction. However, the molecular mechanisms of action whether its intracellular role contributes to atherogenesis remain unclear. Using several databases bulk single cell RNAseq, we first show that Gal3 transcripts are upregulated during plaque progression particular...
Previous studies have demonstrated that a high-protein diet leads to increased atherosclerosis in mice, and this adverse effect is caused by activation of macrophage mTORC1 signaling. Here, we provide detailed protocol for the evaluation diet-induced signaling plaque macrophages atherosclerosis-prone apolipoprotein E (ApoE) knockout (KO) mice. This includes flow cytometry immunofluorescence analysis atherosclerotic can be used study atherogenic potential variety modulators. For complete...
The mechanistic target of rapamycin (mTOR) pathway is considered a key regulator cellular proliferation, survival, metabolism, and degradation. Yet its role in atherosclerosis macrophages the atherosclerotic plaque remains poorly understood. Our previous study has demonstrated macrophage mTORC1 signaling promotes atherogenesis through inhibiting autophagy increasing apoptosis. Using macrophage-specific Rictor- mTOR-deficient mice, we now dissect distinct functions mTORC2 pathways...
Dysfunction in macrophage lysosomes leading to poor handling of atherogenic lipids, apoptotic cells, and other cytotoxic debris leads progression atherosclerotic plaque size complexity. Stimulation TFEB, the master transcriptional regulator autophagy-lysosomal biogenesis, macrophages has been shown promote degradative capacity with reductions atherosclerosis. Thus, there is interest harnessing this pathway for cardiovascular therapeutics. One mechanisms by which TFEB activated triggered...
High-protein intake is common in Western societies and generally considered healthy. However, results from some epidemiological studies suggest elevated protein associated with increased risk for ischemic cardiovascular diseases. In addition, conducted mice show that a high protein, compared standard diet, increases atherosclerosis burden lesion complexity. The adverse effect of ingestion on plaque biology mediated by amino acid-mammalian target rapamycin (mTOR)-dependent inhibition...