Cholic Acid Attenuates ER Stress-Induced Cell Death in Coxsackievirus-B3 Infection

Han, Jae‐Young; Jeong, Hae In; Park, Cheol Woo; Yoon, Jisoo; Ko, Jaeyoung; Nam, Sang‐Jip; Lim, Byung-Kwan

doi:10.4014/jmb.1708.08009

Cited by 13 publications

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“…Cholic acid may influence cardiac electrophysiology, inhibiting the activity of cardiac myocytes, causing calcium overload, and leading to sudden fetal death, and hence might influence cardiac electrophysiology [48]. Furthermore, it has been reported that cholic acid could strongly reduce endoplasmic reticulum stress by inhibiting extracellular signal−regulated kinase signaling and endoplasmic reticulum stress−related activating transcription factor 4 [49]. A 20-year cohort study following >74,000 participants revealed that oleic acid consumption significantly relieved the risk for developing CVD [50].…”

Section: Resultsmentioning

confidence: 99%

Disordered gut microbiota and alterations in metabolic patterns are associated with atrial fibrillation

et al. 2019

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Background With the establishment of the heart-gut axis concept, accumulating studies suggest that the gut microbiome plays an important role in the pathogenesis of cardiovascular diseases. Yet, little evidence has been reported in characterizing the gut microbiota shift in atrial fibrillation. Methods We include the result of the global alterations that occur in the intestinal microbiota in a cohort of 50 patients with atrial fibrillation and 50 matched controls based on a strategy of metagenomic and metabolomic analyses. Results The alterations include a dramatic elevation in microbial diversity and a specific perturbation of gut microbiota composition. Overgrowth of Ruminococcus , Streptococcus , and Enterococcus , as well as reduction of Faecalibacterium , Alistipes , Oscillibacter , and Bilophila were detected in patients with atrial fibrillation. A gut microbial function imbalance and correlated metabolic pattern changes were observed with atrial fibrillation in both fecal and serum samples. The differential gut microbiome signatures could be used to identify patients with atrial fibrillation. Conclusions Our findings characterize the disordered gut microbiota and microbial metabolite profiles in atrial fibrillation. Further research could determine whether intervention strategies targeting intestinal microbiome composition might be useful to counteract the progression of atrial fibrillation.

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Section: Resultsmentioning

confidence: 99%

Disordered gut microbiota and alterations in metabolic patterns are associated with atrial fibrillation

et al. 2019

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“…A study revealed that CDCA markedly decreased rotavirus replication both in vitro and in vivo ( 32 ). Moreover, CA has been found to inhibit the replication, proliferation, and infection of Coxsackievirus-B3 ( 33 ). It has been discovered that the conjugated bile acids of TCDCA and GCDCA exhibit antiviral activity against cytomegalovirus replication ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Alterations in bile acids as metabolic signatures in the patients with human adenovirus type 7 infection

Du²,

Wei³

et al. 2022

Front. Med.

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ObjectivesThe changes in metabolism by human adenovirus (HAdV) infection was unclear. The potential mechanism of HAdV-7 causing acute respiratory tract infection was explored.MethodsTotally 35 patients with HAdV-7 infection, 32 asymptomatic cases with HAdV-7 and 14 healthy controls were enrolled from an outbreak of HAdV-7 in the army. The serum samples were analyzed by untargeted and targeted metabolomics. The effects of differential metabolites were verified on HAdV-7 replication in an A549 cell line.ResultsThe untargeted metabolomics analysis revealed more significant changes in the classes of sphingolipids, polyketides, glycerolipids, fatty acyls, and carboxylic acids and their derivatives in the patients with HAdV-7 than in healthy controls. Two key metabolic pathways of secondary and primary bile acid biosynthesis were noted from pathway enrichment analysis. Targeted metabolomics analysis showed that the levels of unconjugated bile acids in the patients were significantly lower, while the levels of glyco- and tauro- conjugated bile acids in patients and asymptomatic cases were higher than those in the healthy controls. The profiles of cytokines and peripheral lymphocyte subsets obviously varied at different levels of bile acids, with significant differences after HAdV-7 infection. A cell verification test demonstrated that the replication of HAdV-7 significantly reduced when GCDCA and TCA were added.ConclusionBile acids inhibited HAdV-7 replication in vitro. Alterations in bile acids was metabolic signatures of HAdV-7 infected subjects, and our results suggested bile acids might play protective roles against HAdV-7 infection.

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“…As most patients are reported to exhibit abnormal liver functions 1,57 , GOT1 and TKT could serve as potential targets for mitigating hepatic symptoms. The downregulation of cholic acid in patients' plasma indicates reduced fat absorption and cholesterol excretion 58,59 . This metabolic change may also affect the dysregulation of other carbohydrate metabolism pathways, which is supported by elevated levels of lactate and deoxyribose 5-phosphate as well as reduced levels of glycerol-3-phosphate (Supplementary Fig 5B -D).…”

Section: Elevated Acylcarnitines and Relevant Proteomics Alternations Suggest Potential Interruption Of Lipid Transportmentioning

confidence: 99%

Integration and comparison of multi-omics profiles of NGLY1 deficiency plasma and cellular models to identify clinically relevant molecular phenotypes

Chen

Wang

Shen

et al. 2021

Preprint

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NGLY1 (N-glycanase 1) deficiency is a rare congenital recessive disorder caused by a mutation in the NGLY1 gene, which encodes the cytosol enzyme N-glycanase 1. The NGLY1 protein catalyzes the first step in protein deglycosylation, a process prerequisite for the cytosolic degradation of misfolded glycoproteins. By performing and combining metabolomics and proteomics profiles, we showed that NGLY1 deficiency induced the activation of immune response, disturbed lipid metabolism, biogenic amine synthesis and glutathione metabolism. The discovery was further validated by profiling of patient-derived induced pluripotent stem cells (iPSCs) and differentiated neural progenitor cells (NPCs), which serve as a personalized cellular model of the disease. This study provides new insights into the NGLY1 deficiency pathology and demonstrates that the upregulation of immune response and downregulation of lipid metabolism appear to be important molecular phenotypes of NGLY1 deficiency, together with the dysregulation of amino acid metabolism, biogenic amine synthesis and diverse signaling pathways, likely causing broad downstream syndromes. Collectively, such valuable multi-omics profiles identified broad molecular associations of potential pathological mechanisms during the onset of NGLY1 deficiency and suggested potential therapeutic targets for researchers and clinicians.

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Cholic Acid Attenuates ER Stress-Induced Cell Death in Coxsackievirus-B3 Infection

Cited by 13 publications

References 0 publications

Disordered gut microbiota and alterations in metabolic patterns are associated with atrial fibrillation

Disordered gut microbiota and alterations in metabolic patterns are associated with atrial fibrillation

Alterations in bile acids as metabolic signatures in the patients with human adenovirus type 7 infection

Integration and comparison of multi-omics profiles of NGLY1 deficiency plasma and cellular models to identify clinically relevant molecular phenotypes

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