Category: 97-67-6

Yang, Nanmu published the artcileHBXIP drives metabolic reprogramming in hepatocellular carcinoma cells via METTL3-mediated m6A modification of HIF-1α, Synthetic Route of 97-67-6, the main research area is hepatocellular carcinoma HBXIP METTL3 m6A HIF1alpha hepatocyte prognosis; HBXIP; HIF-1α; METTL3; N6-methyladenosine methylation; hepatocellular carcinoma.

Cancer cells sustain high levels of glycolysis and glutaminolysis via reprogramming of intracellular metabolism, which represents a driver of hepatocellular carcinoma (HCC) progression. Understanding the mechanisms of cell metabolic reprogramming may present a new basis for liver cancer treatment. Herein, we collected HCC tissues and noncancerous liver tissues and found hepatitis B virus X-interacting protein (HBXIP) was found to be upregulated in HCC tissues and associated with poor prognosis. The N6-methyladenosine (m6A) level of hypoxia-inducible factor-1α (HIF-1α) in HCC cells was evaluated after the intervention of METTL3. The possible m6A site of HIF-1α was queried and the binding relationship between METTL3 and HIF-1α was verified. The interference of HBXIP suppressed HCC malignant behaviors and inhibited the Warburg effect in HCC cells. METTL3 was upregulated in HCC tissues and pos. regulated by HBXIP. Overexpression of METTL3 restored cell metabolic reprogramming in HCC cells with partial loss of HBXIP. HBXIP mediated METTL3 to promote the metabolic reprogramming and malignant biol. behaviors of HCC cells. The levels of total m6A in HCC cells and m6A in HIF-1α were increased. METTL3 had a binding relationship with HIF-1α and mediated the m6A modification of HIF-1α. In conclusion, HBXIP drives metabolic reprogramming in HCC cells via METTL3-mediated m6A modification of HIF-1α.

Journal of Cellular Physiology published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Synthetic Route of 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Garcia-Caballero, Melissa published the artcileRole and therapeutic potential of dietary ketone bodies in lymph vessel growth, Safety of (S)-2-hydroxysuccinic acid, the main research area is dietary ketone body lymph vessel growth therapeutics.

Abstract: Lymphatic vessels (LVs), lined by lymphatic endothelial cells (LECs), are indispensable for life1. However, the role of metabolism in LECs has been incompletely elucidated. In the present study, it is reported that LEC-specific loss of OXCT1, a key enzyme of ketone body oxidation2, reduces LEC proliferation, migration and vessel sprouting in vitro and impairs lymphangiogenesis in development and disease in Prox1ΔOXCT1 mice. Mechanistically, OXCT1 silencing lowers acetyl-CoA levels, tricarboxylic acid cycle metabolite pools, and nucleotide precursor and deoxynucleotide triphosphate levels required for LEC proliferation. Ketone body supplementation to LECs induces the opposite effects. Notably, elevation of lymph ketone body levels by a high-fat, low-carbohydrate ketogenic diet or by administration of the ketone body β-hydroxybutyrate increases lymphangiogenesis after corneal injury and myocardial infarction. Intriguingly, in a mouse model of microsurgical ablation of LVs in the tail, which repeats features of acquired lymphoedema in humans, the ketogenic diet improves LV function and growth, reduces infiltration of anti-lymphangiogenic immune cells and decreases edema, suggesting a novel dietary therapeutic opportunity.

Nature Metabolism published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Safety of (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Miniero, Daniela Valeria published the artcileThe Interaction of Hemin, a Porphyrin Derivative, with the Purified Rat Brain 2-Oxoglutarate Carrier, Product Details of C4H6O5, the main research area is hemin porphyrin derivative rat brain oxoglutarate carrier; induced-fit molecular docking; inhibition; kinetic study; mitochondrial carrier; porphyrin derivatives; single binding centre gated pore mechanism.

The mitochondrial 2-oxoglutarate carrier (OGC), isolated and purified from rat brain mitochondria, was reconstituted into proteoliposomes to study the interaction with hemin, a porphyrin derivative, which may result from the breakdown of heme-containing proteins and plays a key role in several metabolic pathways. By kinetic approaches, on the basis of the single binding center gated pore mechanism, we analyzed the effect of hemin on the transport rate of OGC in uptake and efflux experiments in proteoliposomes reconstituted in the presence of the substrate 2-oxoglutarate. Overall, our exptl. data fit the hypothesis that hemin operates a competitive inhibition in the 0.5-10 μM concentration range. As a consequence of the OGC inhibition, the malate/aspartate shuttle might be impaired, causing an alteration of mitochondrial function. Hence, considering that the metabolism of porphyrins implies both cytoplasmic and mitochondrial processes, OGC may participate in the regulation of porphyrin derivatives availability and the related metabolic pathways that depend on them (such as oxidative phosphorylation and apoptosis). For the sake of clarity, a simplified model based on induced-fit mol. docking supported the in vitro transport assays findings that hemin was as good as 2-oxoglutarate to bind the carrier by engaging specific ionic hydrogen bond interactions with a number of key residues known for participating in the similarly located mitochondrial carrier substrate binding site.

Biomolecules published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Product Details of C4H6O5.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Giordano, Luca published the artcileAlternative oxidase attenuates cigarette smoke-induced lung dysfunction and tissue damage, Application of (S)-2-hydroxysuccinic acid, the main research area is lung dysfunction tissue damage cigarette smoke alternative oxidase; COPD; alternative oxidase; cigarette smoke; mitochondria.

Cigarette smoke (CS) exposure is the predominant risk factor for the development of chronic obstructive pulmonary disease (COPD) and the third leading cause of death worldwide. We aimed to elucidate whether mitochondrial respiratory inhibition and oxidative stress are triggers in its etiol. In different models of CS exposure, we investigated the effect on lung remodeling and cell signaling of restoring mitochondrial respiratory electron flow using alternative oxidase (AOX), which bypasses the cytochrome segment of the respiratory chain. AOX attenuated CS-induced lung tissue destruction and loss of function in mice exposed chronically to CS for 9 mo. It preserved the cell viability of isolated mouse embryonic fibroblasts treated with CS condensate, limited the induction of apoptosis, and decreased the production of reactive oxygen species (ROS). In contrast, the early phase inflammatory response induced by acute CS exposure of mouse lung, i.e., infiltration by macrophages and neutrophils and adverse signaling, was unaffected. The use of AOX allowed us to obtain novel pathomechanistic insights into CS-induced cell damage, mitochondrial ROS production, and lung remodeling. Our findings implicate mitochondrial respiratory inhibition as a key pathogenic mechanism of CS toxicity in the lung. We propose AOX as a novel tool to study CS-related lung remodeling and potentially to counteract CS-induced ROS production and cell damage.

American Journal of Respiratory Cell and Molecular Biology published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Application of (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Qi, Zihe published the artcileEnhanced Cytotoxicity of Cadmium by a Sulfated Polysaccharide from Abalone, Product Details of C4H6O5, the main research area is cytotoxicity cadmium sulfated polysaccharide abalone lipid metabolism disorder; abalone gonadal polysaccharide; apoptosis; cadmium ion; cell cycle; lipidomics; metabolism.

Consumption of seafood is a common route of cadmium ion (Cd2+) exposure to consumers. The seafood matrixes may alter the toxicity profile of Cd2+ due to the interaction between Cd2+ and biomacromols. in seafood. In this study, enhanced cytotoxicity of Cd2+ was found in the presence of an abalone gonad sulfated polysaccharide (AGSP) and the mechanism was investigated at a metabolic level. The formation of the AGSP-Cd2+ complex was demonstrated by isothermal titration calorimetry. The level of reactive oxygen species (ROS) increased and mitochondrial membrane potential reduced upon exposure to the AGSP-Cd2+ complex as compared with those of Cd2+ exposure. The decreased cell viability after incubation with the AGSP-Cd2+ complex also suggested enhanced Cd2+ toxicity induced by AGSP. The metabolomics and lipidomics anal. revealed that, compared with the Cd2+ group, the AGSP-Cd2+ downregulated the phospholipid metabolism and resulted in more serious damage in the cellular membrane. The lipid metabolism disorder, in turn, amplified the generation of ROS, leading to a decrease in cell viability. These results provided new evidence of the enhanced Cd2+ toxicity upon interaction with seafood polysaccharides, and much attention should be paid to the effect of food ingredients on heavy metal ion toxicity.

Journal of Agricultural and Food Chemistry published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Product Details of C4H6O5.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Cheng, Shih-Chun published the artcileMetabolomic biomarkers in cervicovaginal fluid for detecting endometrial cancer through nuclear magnetic resonance spectroscopy, Computed Properties of 97-67-6, the main research area is metabolome biomarker cervicovaginal fluid endometrial cancer NMR spectroscopy; Biomarkers; Endometrial neoplasms; Magnetic resonance spectroscopy; Metabolomics.

Endometrial cancer (EC) is one of the most common gynecol. neoplasms in developed countries but lacks screening biomarkers. We aim to identify and validate metabolomic biomarkers in cervicovaginal fluid (CVF) for detecting EC through NMR (NMR) spectroscopy. We screened 100 women with suspicion of EC and benign gynecol. conditions, and randomized them into the training and independent testing datasets using a 5:1 study design. CVF samples were analyzed using a 600-MHz NMR spectrometer equipped with a cryoprobe. Four machine learning algorithms-support vector machine (SVM), partial least squares discriminant anal. (PLS-DA), random forest (RF), and logistic regression (LR), were applied to develop the model for identifying metabolomic biomarkers in cervicovaginal fluid for EC detection. A total of 54 women were eligible for the final anal., with 21 EC and 33 non-EC. From 29 identified metabolites in cervicovaginal fluid samples, the top-ranking metabolites chosen through SVM, RF and PLS-DA which existed in independent metabolic pathways, i.e. phosphocholine, malate, and asparagine, were selected to build the prediction model. The SVM, PLS-DA, RF, and LR methods all yielded area under the curve values between 0.88 and 0.92 in the training dataset. In the testing dataset, the SVM and RF methods yielded the highest accuracy of 0.78 and the specificity of 0.75 and 0.80, resp. Phosphocholine, asparagine, and malate from cervicovaginal fluid, which were identified and independently validated through models built using machine learning algorithms, are promising metabolomic biomarkers for the detection of EC using NMR spectroscopy.

Metabolomics published new progress about Algorithm. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Computed Properties of 97-67-6.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Torres, Maria J. published the artcileIntracardiac administration of ephrinA1-Fc preserves mitochondrial bioenergetics during acute ischemia/reperfusion injury, Product Details of C4H6O5, the main research area is ischemia reperfusion injury intracardiac ephrinA1 mitochondrial bioenergetics; Cardioprotection; Mitochondrial bioenergetics; Myocardial infarction; ephrinA1.

Herein, 10 wk-old B6129SF2/J male mice were exposed to acute ischemia/reperfusion injury immediately followed by intracardiac injection of either EphrinA1-Fc or IgG-Fc. After 24 h of reperfusion, sections of the infarct margin in the left ventricle were imaged via transmission electron microscopy, and mitochondrial function was assessed in both permeabilized fibers and isolated mitochondria, to examine mitochondrial structure, function, and energetics in the early stages of repair. At a structural level, EphrinA1-Fc administration prevented the I/R-induced loss of sarcomere alignment and mitochondrial organization along the Z disks, as well as disorganization of the cristae and loss of inter-mitochondrial junctions. Preservation of cardiac bioenergetics was not due to changes in mitochondrial JH2O2 emitting potential, membrane potential, ADP affinity, efficiency of ATP production, or activity of the main dehydrogenase enzymes, suggesting that EphrinA1-Fc indirectly maintains respiratory function via preservation of the mitochondrial network. Moreover, these protective effects were lost in isolated mitochondria, further emphasizing the importance of the intact cardiomyocyte ultrastructure in mitochondrial energetics. Collectively, these data suggest that intracardiac injection of EphrinA1-Fc protects cardiac function by preserving cardiomyocyte structure and mitochondrial bioenergetics, thus emerging as a potential therapeutic strategy in I/R injury.

Life Sciences published new progress about Apoptosis. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Product Details of C4H6O5.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Feng, Mi published the artcileDirect conversion of shrimp shells to O-acylated chitin with antibacterial and anti-tumor effects by natural deep eutectic solvents, Product Details of C4H6O5, the main research area is shrimp shell acylated chitin antibacterial antitumor deep eutectic solvent.

To obtain O-acylated chitin from shrimp shells directly, the used solvent should have multiple functions to remove calcium carbonate, protein, and acylated chitin. Herein, we use the acidic natural deep eutectic solvents (NADESs) with the ability to release H+ and various hydrogen bonding sites to achieve the above goal. The involved NADESs with three abilities of decalcification, deproteinization and acylation replaced acids, alkalis, catalysts, and acylation reagents in the conventional method. The exptl. results revealed that the components of the NADESs, experiment temperature and time played key roles in the purity and degree of substitution (DS) of O-acylated chitin. Meanwhile, the ratio of shrimp shells to NADESs and a small amount of water had little effect on the preparation of O-acylated chitin. With the optimal NADES (choline chloride/DL-malic acid 1 : 2, ChCl 1-DL Mal 2) treatment under the optimal conditions, the purity of O-malate chitin reached 98.6% with a DS of 0.46, exhibiting antibacterial and anti-tumor effects. The exptl. results showed that the removal of calcium carbonate and protein and acylation of chitin were carried out simultaneously. Mechanistic exploration using spectroscopy and experiments confirmed that H+ release from ChCl 1-DL Mal 2 was the main reason for the removal of calcium carbonate and initiation acylation reaction. The protein was degraded to amino acids because of the acidity of ChCl 1-DL Mal 2 and dissolved in the NADES due to hydrogen bonding formation with ChCl 1-DL Mal 2.

Green Chemistry published new progress about Acylation. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Product Details of C4H6O5.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

D’souza, Kenneth published the artcileWhey peptides stimulate differentiation and lipid metabolism in adipocytes and ameliorate lipotoxicity-induced insulin resistance in muscle cells, Recommanded Product: (S)-2-hydroxysuccinic acid, the main research area is whey peptide lipid adipocyte lipotoxicity insulin resistance muscle cell; PPAR; adipocytes; differentiation; insulin resistance; lipolysis; lipotoxicity; metabolism; mitochondria; myocytes; whey peptides.

Deregulation of lipid metabolism and insulin function in muscle and adipose tissue are hallmarks of systemic insulin resistance, which can progress to type 2 diabetes. While previous studies suggested that milk proteins influence systemic glucose homeostasis and insulin function, it remains unclear whether bioactive peptides generated from whey alter lipid metabolism and its accumulation in muscle and adipose tissue. Therefore, we incubated murine 3T3-L1 preadipocytes and C2C12 myotubes with a whey peptide mixture produced through pepsin-pancreatin digestion, mimicking peptides generated in the gut from whey protein hydrolysis, and examined its effect on indicators of lipid metabolism and insulin sensitivity. Whey peptides, particularly those derived from bovine serum albumin (BSA), promoted 3T3-L1 adipocyte differentiation and triacylglycerol (TG) accumulation in accordance with peroxisome proliferator-activated receptor γ (PPARγ) upregulation. Whey/BSA peptides also increased lipolysis and mitochondrial fat oxidation in adipocytes, which was associated with the upregulation of peroxisome proliferator-activated receptor δ (PPARδ). In C2C12 myotubes, whey but not BSA peptides ameliorated palmitate-induced insulin resistance, which was associated with reduced inflammation and diacylglycerol accumulation, and increased sequestration of fatty acids in the TG pool. Taken together, our study suggests that whey peptides generated via pepsin-pancreatin digestion profoundly alter lipid metabolism and accumulation in adipocytes and skeletal myotubes.

Nutrients published new progress about Adipocyte. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Recommanded Product: (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts

Yang, Huan published the artcileSigma-1 receptor ablation impedes adipocyte-like differentiation of mouse embryonic fibroblasts, Safety of (S)-2-hydroxysuccinic acid, the main research area is sigma 1 adipocyte differentiation embryonic fibroblast; Adipogenic induction; Body weight gain; Mouse embryonic fibroblast; Sigma-1 receptor.

The sigma-1 receptor (Sig1R) is a unique ligand-operated endoplasmic reticulum (ER) protein without any mammalian homolog. It has long been a pharmacol. target for intervention of psychiatric disorders, and recently garnered refreshed interest for its neuroprotective potential. Though reported to modulate various intracellular events, its influence on cell identity is little known. We explored a role for Sig1R in adipocyte differentiation. We induced adipogenic differentiation of mouse embryonic fibroblasts (MEFs) with a differentiation medium. MEFs were isolated from Sigmar1-/- and Sigmar1+/+ mice. The induced adipocyte-like phenotype was detected through Western blots of master transcription factors (PPARγ, CEBPA, SREBP1, SREBP2), lipogenic proteins (FABP4, ACC1, ACAT2), and Oil-Red-O staining of lipids. We found that the induced upregulation of these proteins and lipid accumulation were severely mitigated in Sigmar1-/- (vs Sigmar1+/+) MEFs. Sig1R activation with a selective agonist (PRE084) increased Sig1R protein and further enhanced the induced adipocyte-like phenotype in Sigmar1+/+ MEFs. We also determined mouse body weight gain induced by high-fat diet for 6 mo, which was impeded in Sigmar1-/- (vs Sigmar1+/+) male mice. In summary, genetic ablation of Sig1R impairs, and agonist activation of Sig1R enhances adipocyte-like phenotype of induced MEFs. In vivo, Sig1R ablation impedes the body weight gain of male mice on high-fat diet. This study warrants further investigation of a previously unrecognized role for Sig1R in adipocyte differentiation.

Cellular Signalling published new progress about Adipocyte. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Safety of (S)-2-hydroxysuccinic acid.

Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts