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The plasma lipidomic signature of nonalcoholic steatohepatitis
TLDR
Although increased lipogenesis, desaturases, and LOX activities characterize NAFL and NASH, impaired peroxisomal polyunsaturated fatty acid (PUFA) metabolism and nonenzymatic oxidation is associated with progression to NASH.
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
TLDR
There continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes, so it is important to update guidelines for monitoring autophagic activity in different organisms.
Bile acids as regulatory molecules
TLDR
Current knowledge of how bile acids regulate hepatic lipid and glucose metabolism through the activation of specific nuclear receptors and cell signaling pathways is summarized.
Increased hepatic synthesis and dysregulation of cholesterol metabolism is associated with the severity of nonalcoholic fatty liver disease.
TLDR
Dysregulated cholesterol metabolism in NAFLD is demonstrated which may contribute to disease severity and cardiovascular risks and is associated with increased SREBP-2 maturation, HMG CoA reductase (HMGCR) expression and decreased phosphorylation of HMGCR.
Prostaglandin catabolizing enzymes.
The primary catabolic pathway of prostaglandins and related eicosanoids is initiated by the oxidation of 15(S)-hydroxyl group catalyzed by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase
Inhibition of sustained smooth muscle contraction by PKA and PKG preferentially mediated by phosphorylation of RhoA.
TLDR
Results demonstrate that dephosphorylation of MLC(20) and smooth muscle relaxation are preferentially mediated by PKG- and PKA-dependent phosphorylation and inactivation of RhoA.
Conjugated bile acids activate the sphingosine‐1‐phosphate receptor 2 in primary rodent hepatocytes
TLDR
All these data support the hypothesis that conjugated bile acids activate the ERK1/2 and AKT signaling pathways primarily through S1P2 in primary rodent hepatocytes.
Flavonoid Apigenin Inhibits Lipopolysaccharide-Induced Inflammatory Response through Multiple Mechanisms in Macrophages
TLDR
The results indicated that apigenin significantly inhibited LPS-induced production of pro-inflammatory cytokines, such as IL-6, IL-1β, and TNF-α through modulating multiple intracellular signaling pathways in macrophages.
Bile acids are nutrient signaling hormones
Bile salts play crucial roles in allowing the gastrointestinal system to digest, transport and metabolize nutrients. They function as nutrient signaling hormones by activating specific nuclear
Distinctive G protein-dependent signaling in smooth muscle by sphingosine 1-phosphate receptors S1P1 and S1P2.
TLDR
S1P induces initial contraction mediated by S1P(2) and S2P(1) involving concurrent activation of PLC-beta1 and P LC-beta3 via Galpha(q) and Gbetagamma(i), resulting in inositol 1,4,5-trisphosphate-dependent Ca(2+) release and MLCK-mediated MLC(20) phosphorylation.
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