Purinergic receptor P2Y12 boosts autoimmune hepatitis through hexokinase 2-dependent glycolysis in T cells

Zhuang, Wei; Liu, Xiucheng; Li, Guangyu; Lü, Jie; Qin, Hao; Wang, Chun; Xie, Lin; Saimaier, Kaidireya; Han, Sanxing; Shi, Changjie; Hua, Qiuhong; Zhang, Ru; Du, Changsheng

doi:10.7150/ijbs.85133

Cited by 2 publications

(1 citation statement)

References 56 publications

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“…SLAMF7 [226], GPR174 [227], FCRL3 [228], SLAMF6 [229], EOMES (eomesodermin) [230], CCR4 [231], CCR2 [232], CD48 [233], CD3E [234], CCL26 [235], CCL4 [236], SLAMF1 [237], CD24 [238], IKZF3 [239], CD2 [240], CD28 [241], IL7R [242], FCGR2B [243], UBASH3A [244], CD1C [245], ICOS (inducible T cell costimulator) [246], CD3G [247], CCL3 [248], LTF (lactotransferrin) [249], GPNMB (glycoprotein nmb) [250], CTLA4 [251], IRF4 [252], TNFRSF9 [253], FCRL5 [254], LAIR2 [255], TAB2 [256], CD52 [257], CD163 [258], MSR1 [259], HGF (hepatocyte growth factor) [260], SIGLEC1 [261], TTR (transthyretin) [262], IL24 [263], IL9 [264], CHI3L1 [265], CDH1 [266], OLIG2 [267], NKX6-2 [268]. HK2 [269], PNPLA3 [270], CPB2 [271], SEMA4C [272], LRP2 [273], SLC5A11 [274], F11 [275], ANGPTL2 [276] and CYP2A6 [277] genes might be related to the pathophysiology of autoimmune disease. A recent study revealed that SLAMF7 [278], FCRL3 [279], CCR4 [280], GZMA (granzyme A) [281], CCR2 [282], CD48 [283], CD3E [284], CCL4 [285], FASLG (Fas ligand) [286], SLAMF1 [287], CD28 [288], IL7R [289], UBASH3A [290], CD3D [291], ICOS (inducible T cell costimulator) [292], CCL5 [293], CCL3 [294], LTF (lactotransferrin) [295], CTLA4 [296], TNFRSF9 [253], C6 [297], IL5RA [298], IL2RG […”

Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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Multiple sclerosis (MS) is the main reason for disability caused by autoimmunity. However, effective biomarkers for MS have not been identified. This study explored the molecular mechanisms and potential therapeutic targets for MS occurrence and progression using bioinformatics and next generation sequencing (NGS) data analysis. NGS data GSE138614, including patients with MS and 25 normal control samples, were obtained from Gene Expression Omnibus (GEO) database Differentially expressed genes (DEGs) were filtered and subjected to gene ontology (GO) and pathway enrichment analyses. Protein–protein interaction (PPI) network and module analyses were performed based on the DEGs. MiRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were built by Cytoscape to predict the underlying microRNAs (miRNAs) and transcription factors (TFs) associated with hub genes. We also validated the identified hub genes via receiver operating characteristic (ROC) curve analysis. A total of 959 DEGs (479 up regulated genes and 480 down regulated genes) were detected. The GO terms and pathways of DEGs involve immune system process, developmental process, immune system and regulation of cholesterol biosynthesis by SREBP (SREBF). The network analysis revealed that hub genes include LCK, PYHIN1, SLAMF1, DOK2, TAB2, CFTR, RHOB, LMNA, EGLN3 and ERBB3 might be involved in the development of MS. The present investigation illustrates a characteristic gene profile in MS, which might contribute to the interpretation of the progression of MS and provide novel biomarkers and therapeutic targets for MS.

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Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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Prospective Coronavirus Liver Effects: Available Knowledge

Avishek

2023

Ann Clin Gastroenterol Hepatol

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The global pandemic COVID-19, caused by SARS-CoV-2, affected millions of people. COVID-19 is known for its respiratory symptoms, but new research reveals it may also affect other organ systems, including the liver. This abstract reviews COVID-19 and liver function. The virus enters host cells through liver-expressed angiotensin-converting enzyme 2 (ACE2) receptors. Thus, viral infection and replication may target the liver. Virus-induced inflammation and cytokine production may also harm the liver. ALT and AST elevations are the most prevalent liver abnormalities in COVID-19 patients. Liver function test abnormalities frequently indicate serious illness and poor clinical outcomes. COVID-19 may worsen pre-existing liver diseases such as NAFLD and chronic viral hepatitis. Drug-induced liver damage (DILI) from COVID-19 therapies including antivirals and corticosteroids complicates liver complications care. Recent investigations have also shown that COVID-19 may cause long-term liver damage. In conclusion, COVID-19 infection, immune-mediated damage, and treatment problems may severely compromise liver function. Optimizing patient treatment and discovering targeted medicines requires understanding COVID-19's liver role. To reduce the effects of COVID-19 on liver function, further study is required to understand the mechanisms and long-term effects.

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Purinergic receptor P2Y12 boosts autoimmune hepatitis through hexokinase 2-dependent glycolysis in T cells

Cited by 2 publications

References 56 publications

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Prospective Coronavirus Liver Effects: Available Knowledge

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