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4 results on '"STAT, signal transducers and activators of transcription"'

1. Clinical efficacies, underlying mechanisms and molecular targets of Chinese medicines for diabetic nephropathy treatment and management

Author

Hai-Yong Chen, Yibin Feng, Cheng Zhang, Ning Wang, Sha Li, and Guoyi Tang

Subjects
LOX1, lectin-like oxidized LDL receptor 1, BUN, blood urea nitrogen, TGBM, thickness of glomerular basement membrane, NQO1, NAD(P)H:quinone oxidoreductase 1, STAT, signal transducers and activators of transcription, N/O, not observed, p62, sequestosome 1 protein, p-IRS1, phospho-IRS1, Review, NOX-4, nicotinamide adenine dinucleotide phosphate-oxidase-4, OCP, oxidative carbonyl protein, Traditional Chinese medicine, AGEs, advanced glycation end-products, N/A, not applicable, TRAF5, tumor-necrosis factor receptor-associated factor 5, Health problems, 0302 clinical medicine, ESRD, end-stage renal disease, LDL, low-density lipoprotein, BMP-7, bone morphogenetic protein-7, TGFβR-I/II, TGF-β receptor I/II, Medicine, P70S6K, 70-kDa ribosomal protein S6 kinase, General Pharmacology, Toxicology and Pharmaceutics, SOCS, suppressor of cytokine signaling proteins, HO-1, heme oxygenase-1, 0303 health sciences, TG, triglyceride, BW, body weight, HDL-C, high density lipoprotein-cholesterol, RASI, renin-angiotensin system inhibitor, ATK, protein kinase B, TBARS, thiobarbituric acid-reactive substance, BCL-XL, B-cell lymphoma-extra large, Gαq, Gq protein alpha subunit, GCK, glucokinase, PI3K, phosphatidylinositol 3 kinases, Systematic review, TLR-2/4, toll-like receptor 2/4, IR, insulin receptor, PERK, protein kinase RNA-like eukaryotic initiation factor 2A kinase, 030220 oncology & carcinogenesis, CRP, C-reactive protein, IRS, insulin receptor substrate, AM, mesangial area, JAK, Janus kinase, FBG, fasting blood glucose, ETAR, endothelium A receptor, LDL-C, low density lipoprotein-cholesterol, CD2AP, CD2-associated protein, eIF2α, eukaryotic initiation factor 2α, RM1-950, mTOR, mammalian target of rapamycin, CHOP, C/EBP homologous protein, STZ, streptozotocin, 03 medical and health sciences, ADE, adverse event, PKC, protein kinase C, LC3, microtubule-associated protein light chain 3, ORP150, 150-kDa oxygen-regulated protein, PGE2, prostaglandin E2, IL-1β/6, interleukin 1β/6, Diabetic kidney disease, IGF-1, insulin-like growth factor 1, EP, E-prostanoid receptor, FN, fibronectin, eGFR, estimated GFR, MDA, malondialdehyde, Chinese medicine, MMP-2, matrix metallopeptidase 2, XBP-1, spliced X box-binding protein 1, TGF-β, tumor growth factor β, GRB 10, growth factor receptor-bound protein 10, medicine.disease, Clinical trial, GRP78, glucose-regulated protein 78, UP, urinary protein, IGF-1R, insulin-like growth factor 1 receptor, ACEI, angiotensin-converting enzyme inhibitor, BCL-2, B-cell lymphoma 2, EMT, epithelial-to-mesenchymal transition, MAPK, mitogen-activated protein kinase, MYD88, myeloid differentiation primary response 88, PBG, postprandial blood glucose, RCT, randomized clinical trial, N/R, not reported, COL-I/IV, collagen I/IV, PINK1, PTEN-induced putative kinase 1, UACR, urinary albumin to creatinine ratio, C, control group, Diabetic nephropathy, GPX, glutathione peroxidase, ICAM-1, intercellular adhesion molecule-1, Bioinformatics, VCAM-1, vascular cell adhesion molecule-1, AMPKα, adenosine monophosphate-activated protein kinase α, DM, diabetes mellitus, TFEB, transcription factor EB, TNF-α, tumor necrosis factor α, Molecular target, IKK-β, IκB kinase β, Signaling pathway, GLUT4, glucose transporter type 4, BAX, BCL-2-associated X protein, NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells, PARP, poly(ADP-Ribose) polymerase, SMURF-2, SMAD ubiquitination regulatory factor 2, AREs, antioxidant response elements, MD, mean difference, SMAD, small mothers against decapentaplegic, MCP-1, monocyte chemotactic protein-1, VEGF, vascular endothelial growth factor, cAMP, cyclic adenosine monophosphate, ARB, angiotensin receptor blocker, PAI-1, plasminogen activator inhibitor-1, SMD, standard mean difference, JNK, c-Jun N-terminal kinase, NRF2, nuclear factor erythroid 2-related factor 2, IκB-α, inhibitory protein α, Herbal medicine, TCM, traditional Chinese medicine, DG, glomerular diameter, GSK-3, glycogen synthase kinase 3, SIRT1, sirtuin 1, D, duration, HbA1c, glycosylated hemoglobin, WMD, weight mean difference, CTGF, connective tissue growth factor, ER, endoplasmic reticulum, DN, diabetic nephropathy, ROS, reactive oxygen species, CCR, creatinine clearance rate, SOD, superoxide dismutase, Diabetes mellitus, PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1α, ET-1, endothelin-1, UMA, urinary microalbumin, SCr, serum creatinine, IRE-1α, inositol-requiring enzyme-1α, 030304 developmental biology, TII, tubulointerstitial injury index, RAGE, receptors of AGE, business.industry, GFR, glomerular filtration rate, PTEN, phosphatase and tensin homolog, CI, confidence interval, TC, total cholesterol, SD-rat, Sprague–Dawley rat, UAER, urinary albumin excretion rate, DKD, diabetic kidney disease, T, treatment group, Molecular targets, Therapeutics. Pharmacology, α-SMA, α smooth muscle actin, SD, standard deviation, business, DAG, diacylglycerol, GCLC, glutamate-cysteine ligase catalytic subunit, Kidney disease
Abstract

Diabetic nephropathy (DN) has been recognized as a severe complication of diabetes mellitus and a dominant pathogeny of end-stage kidney disease, which causes serious health problems and great financial burden to human society worldwide. Conventional strategies, such as renin-angiotensin-aldosterone system blockade, blood glucose level control, and bodyweight reduction, may not achieve satisfactory outcomes in many clinical practices for DN management. Notably, due to the multi-target function, Chinese medicine possesses promising clinical benefits as primary or alternative therapies for DN treatment. Increasing studies have emphasized identifying bioactive compounds and molecular mechanisms of reno-protective effects of Chinese medicines. Signaling pathways involved in glucose/lipid metabolism regulation, antioxidation, anti-inflammation, anti-fibrosis, and podocyte protection have been identified as crucial mechanisms of action. Herein, we summarize the clinical efficacies of Chinese medicines and their bioactive components in treating and managing DN after reviewing the results demonstrated in clinical trials, systematic reviews, and meta-analyses, with a thorough discussion on the relative underlying mechanisms and molecular targets reported in animal and cellular experiments. We aim to provide comprehensive insights into the protective effects of Chinese medicines against DN., Graphical abstract Diabetic nephropathy is one of the most severe complications of diabetes mellitus. Chinese medicines have been intensively studied in treating diabetic nephropathy. This review comprehensively summarizes and discusses the clinical efficacies and underlying mechanisms of Chinese medicines for diabetic nephropathy, providing deep insights and profound perspectives into this field.Image 1

Published
2021
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2. Mettl14-Mediated m6A Modification Facilitates Liver Regeneration by Maintaining Endoplasmic Reticulum Homeostasis

Author

Mingyang Shao, Qing Xu, Menglin Chen, Xiaoyue Cao, Chuan Li, Hong Bu, Yuwei Chen, Yuke Shu, Zhenru Wu, Gang Guo, Yuping Gong, Yongjie Zhou, and Yujun Shi

Subjects
Male, 0301 basic medicine, Adenosine, FoxM1, forkhead box M1, IRE1α, inositol requiring enzyme 1 alpha, XBP1, X-box-binding protein 1, STAT, signal transducers and activators of transcription, RNA Stability, Mettl3, methyltransferase-like 3, Alkbh5, ALKB family member 5 protein, Apoptosis, RC799-869, AST, aspartate aminotransferase, WTAP, Wilms’ tumor 1-associated protein, Endoplasmic Reticulum, UPR, unfolded protein response, 0302 clinical medicine, ERK, extracellular signal-regulated kinase, Homeostasis, TUDCA, tauroursodeoxycholate, BrdU, 5-bromo-2-deoxyuridine, eIF2α, eukaryotic translation initiator factor 2α, Original Research, Mice, Knockout, N6-methyladenosine, Chemistry, Gastroenterology, PI3K, phosphatidylinositol 3-kinase, Methylation, Diseases of the digestive system. Gastroenterology, Cell cycle, Endoplasmic Reticulum Stress, Liver regeneration, Cell biology, UTR, untranslated region, medicine.anatomical_structure, Liver, PHx, partial hepatectomy, Organ Specificity, Hepatocyte, qPCR, quantitative polymerase chain reaction, 030211 gastroenterology & hepatology, FTO, fat mass and obesity-associated protein, ATF6, activating transcription factor 6, AMPK, adenosine 5′-monophosphate-activated protein kinase, JAK, janus kinase, ER, endoplasmic reticulum, Taurochenodeoxycholic Acid, PAS, periodic acid–Schiff, Necrosis, 03 medical and health sciences, ALT, alanine aminotransferase, TM, tunicamycin, medicine, Act D, actinomycin, Animals, Hepatectomy, RNA, Messenger, Cell Proliferation, Messenger RNA, Hepatology, Endoplasmic reticulum, CDS, coding sequence, Mettl14, Methyltransferases, FC, fold change, m6A, N6-methyladenosine, WT, wild-type, Liver Regeneration, m6A-seq, m6A sequencing, 030104 developmental biology, MRNA Sequencing, Hepatocytes, Unfolded protein response, EIF3A, eukaryotic translation initiation factor 3 subunit A, HCC, hepatocellular carcinoma, Peptides, Transcriptome, PERK, protein kinase R-like endoplasmic reticulum kinase, Chop, C/EBP-homologous protein, MAPK, mitogen-activated protein kinase, Gene Deletion
Abstract

Background & Aims N6-methyladenosine (m6A), the most prevalent and dynamic posttranscriptional methylation modification of mammalian mRNA, is involved in various biological processes, but its role in liver regeneration has not been characterized. Methods We first conducted transcriptome-wide m6A mRNA sequencing and characterized the expression pattern of m6A in regenerating mouse liver. Next, we generated hepatocyte-specific Mettl3- or Mettl14-deficient mice and investigated their role in liver regeneration. A series of biochemical experiments in vitro and in vivo was further performed to investigate potential mechanisms. Results We identified an overwhelming proportion of m6A-modified genes with initially up-regulated and subsequently down-regulated m6A levels as liver regeneration progressed. Loss of Mettl14 but not of Mettl3 resulted in markedly disrupted liver regeneration, and Mettl14-ablated hepatocytes were arrested in the G1 phase of the cell cycle. Most strikingly, the Mettl14-ablated regenerating liver exhibited extensive parenchymal necrosis. mRNA transcripts, such as Hsp90b1, Erp29, Stt3a, P4hb, and Lman1, encoding proteins involved in polypeptide processing and the endoplasmic reticulum (ER) stress response, were m6A-hypomethylated, and their mRNA and protein levels were subsequently decreased, resulting in unresolved ER stress, hepatocyte death, and inhibited proliferation. Conclusions We demonstrate the essential role of Mettl14 in facilitating liver regeneration by modulating polypeptide-processing proteins in the ER in an m6A-dependent manner., Graphical abstract

Published
2021
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3. Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions

Author

Bhaskar Saha, Sara Jafarzadeh, Abdollah Jafarzadeh, Prashant Chauhan, and Maryam Nemati

Subjects
Chemokine, ALI, acute lung injury, STAT, signal transducers and activators of transcription, viruses, medicine.medical_treatment, RIG-I, retinoic acid-inducible gene I, Pathogenesis, Severe Acute Respiratory Syndrome, Monocytes, pDCs, plasmacytoid dendritic cells, PRRs, pattern recognition receptors, Macrophage, Medicine, General Pharmacology, Toxicology and Pharmaceutics, Respiratory Distress Syndrome, biology, General Medicine, MCP-1, monocyte chemoattractant protein-1, MERS-CoV, Middle East respiratory syndrome-related coronavirus, SARS-CoV, severe acute respiratory syndrome-related coronavirus, Cytokine, CRP, C-reactive protein, Cytokines, NLRP3, Nod-like receptor protein 3, Chemokines, Coronavirus Infections, Pneumonia, Viral, CD, cluster of differentiation, NF-κB, nuclear factor-κB, mTOR, mammalian target of rapamycin, ACE2, angiotensin-converting enzyme 2, SARS-CoV-2, severe acute respiratory syndrome coronavirus 2, Article, WHO, World Health Organization, Virus, General Biochemistry, Genetics and Molecular Biology, Betacoronavirus, Immune system, PAMPs, pathogen-associated molecular patterns, Humans, MHC, major histocompatibility complex, IFN, interferon, ADAM17, ADAM metallopeptidase domain 17, Antigen-presenting cell, Pandemics, ARDS, acute respiratory distress syndrome, Inflammation, PBMCs, peripheral blood mononuclear cells, ADCC, antibody-dependent cellular cytotoxicity, SARS-CoV-2, business.industry, Macrophages, fungi, COVID-19, CTL, cytotoxic T lymphocyte, medicine.disease, MDA5, melanoma differentiation-associated protein 5, PRRSV, porcine reproductive and respiratory syndrome virus, Treg, regulatory T cells, siRNA, small interfering RNA, Immunology, biology.protein, TMPRSS2, transmembrane serine protease 2, business, Cytokine storm, IRF, interferon regulatory factor
Abstract

The COVID-19-, SARS- and MERS-related coronaviruses share many genomic and structural similarities. However, the SARS-CoV-2 is less pathogenic than SARS-CoV and MERS-CoV. Despite some differences in the cytokine patterns, it seems that the cytokine storm plays a crucial role in the pathogenesis of COVID-19-, SARS- and MERS. Monocytes and macrophages may be infected by SARS-CoV-2 through ACE2-dependent and ACE2-independent pathways. SARS-CoV-2 can effectively suppress the anti-viral IFN response in monocytes and macrophages. Since macrophages and dendritic cells (DCs) act as antigen presenting cells (APCs), the infection of these cells by SARS-CoV-2 impairs the adaptive immune responses against the virus. Upon infection, monocytes migrate to the tissues where they become infected resident macrophages, allowing viruses to spread through all organs and tissues. The SARS-CoV-2-infected monocytes and macrophages can produce large amounts of numerous types of pro-inflammatory cytokines and chemokines, which contribute to local tissue inflammation and a dangerous systemic inflammatory response called cytokine storm. Both local tissue inflammation and the cytokine storm play a fundamental role in the development of COVID-19-related complications, such as acute respiratory distress syndrome (ARDS), which is a main cause of death in COVID-19 patients. Here, we describe the monocytes and macrophage responses during severe coronavirus infections, while highlighting potential therapeutic interventions to attenuate macrophage-related inflammatory reactions in possible approaches for COVID-19 treatment., Graphical abstract Unlabelled Image, Highlights • A subset of monocytes and macrophages may be infected by SARS-CoV-2. • Coronavirus-infected monocyte can migrate to tissue and become infected macrophage. • Coronavirus-infected monocyte/macrophage produces high level of inflammatory factors. • Monocyte/macrophage-related cytokines promote organ inflammation and cytokine storm. • Local tissue inflammation and cytokine storm cause multi-organ failure in COVID-19.

Published
2020
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4. Anti-malarial drug, artemisinin and its derivatives for the treatment of respiratory diseases

Author

Daniel W.S. Tan, Fred W.S. Wong, Dorothy H.J. Cheong, and Thai Tran

Subjects
CTX, cyclophosphamide, STAT, signal transducers and activators of transcription, Artesunate (PubChem CID:156252), HDAC2, histone deacetylase 2, Pharmacology, Nrf2, nuclear factor erythroid 2-related factor 2, TNF, tumour necrosis factor, SLE, systemic lupus erythematosus, VCAM-1, vascular cell adhesion molecule 1, 0302 clinical medicine, eos, eosinophil, GSH, glutathione, 3-NT, 3-nitrotyrosine, Medicine, IκBα, inhibitor of NF-κB alpha, Th17, T helper 17, HO-1, heme oxygenase-1, ICAM-1, intercellular adhesion molecule 1, chemistry.chemical_classification, XIAP, X-linked inhibitor of apoptosis protein, YKL-40, chitinase-like glycoprotein, Chemical compounds studied in this article Artemisinin (PubChem CID: 68827), MCP-1, monocyte chemoattractant protein-1, HIF-1α, hypoxia-inducible factor 1-alpha, Artemisinins, DHA, dihydroartemisinin, GLUT, glucose transporter, HELF, human embryonic lung fibroblasts, RNAi, RNA interference, VDAC2, voltage-dependent anion channel 2, 030220 oncology & carcinogenesis, COX-2, cyclooxygenase-2, LADPI, liposomal artesunate dry powder inhalers, behavior and behavior mechanisms, iNOS, inducible nitric oxide synthase, IP-10, IFNγ-induced protein 10, 8-iso, 8-isoprostane, psychological phenomena and processes, Foxo1, forkhead box O1, KDR/flk-1, kinase insert domain receptor /fetal liver kinase-1, education, H2AX, H2A histone family member X, PCNA, proliferating cell nuclear antigen, Pneumonia, Viral, MIP-2, macrophage inflammatory protein 2, mTOR, mammalian target of rapamycin, ACE2, angiotensin-converting enzyme 2, Antiviral Agents, Article, 4EBP1, eukaryotic translation initiation factor 4E-binding protein 1, 03 medical and health sciences, LD50, lethal dose, Betacoronavirus, ARTD, artemisinin-daumone hybrid 15, BDHA, biotinylated dihydroartesunate, PGE2, prostaglandin E2, TGF, tumour growth factor, Humans, DHA-NLC, dihydroartemisinin-nanostructured lipid carriers, u-PA, urokinase-type plasminogen activator, TSLP, thymic stromal lymphopoietin, E2F1, E2F transcription factor 1, LLC, lewis lung carcinoma, PEG, polyethylene glycol, MDA, malondialdehyde, NO, nitric oxide, hsp47, heat shock protein 47, Arteether (PubChem CID: 3000469), medicine.disease, IL, interleukin, 030104 developmental biology, Mcl-1, myeloid cell leukemia-1, cell proliferation, chemistry, COPD, chronic obstructive pulmonary disease, Smac, second mitochondrial activator of caspases, Treg, regulatory T, artemisinin, Apoptosis, NQO1, NAD(P)H quinone dehydrogenase 1, CSE, cigarette smoke extract, Malaria, 0301 basic medicine, Lung Diseases, Lymp, lymphocyte, Respiratory diseases, ALI, acute lung injury, DLAedried, leaf artemisia extract, MPO, myeloperoxidase, 8-OHdG, 8-hydroxy-2’-deoxyguanosine, AP-1, activator protein 1, LMVD, lymphatic microvessel density, TLR4, toll-like receptor 4, 2DG, 2-Deoxy-D-glucose, chemistry.chemical_compound, Artemether (PubChem CID: 68911), DNA, deoxyribonucleic acid, SCLC, small cell lung cancer, KC, keratinocyte chemoattractant, BALF, bronchoalveolar lavage fluid, Artemisinin, Rb, retinoblastoma, ABCG2, ATP-binding cassette subfamily member 2, NF-κB, nuclear factor-kappa B, CDK, cyclin-dependent kinase, ATF3, activating transcription factor 3, GPx, glutathione peroxidase, INF, interferon, CDDP, cisplatin, RA, FLS rheumatoid arthritis fibroblast-like synoviocytes, [Ca2+]i, intracellular calcium ion, NOX, NADPH oxidase, RIR, renal ischemia reperfusion, VEGF, vascular endothelial growth factor, Vascular endothelial growth factor, MMP, matrix metalloproteinase, AHR, airway hyperresponsiveness, JNK, c-Jun N-terminal kinase, shRNA, short hairpin RNA, LPS, lipopolysaccharide, medicine.symptom, EMT, epithelial-mesenchymal transition, Coronavirus Infections, NKD2, naked cuticle homolog 2, PI3K, phosphoinositide 3-kinase, Artemisitene (PubChem CID: 11000442), medicine.drug, AEC, alveolar epithelial cells, GSK3β, glycogen synthase kinase 3 beta, NPC, nasopharyngeal carcinoma, ATP, adenosine triphosphate, Dihydroartemisinin (PubChem CID: 139073990), Inflammation, neu, neutrophil, lung, ER, endoplasmic reticulum, OVA, ovalbumin, ROS, reactive oxygen species, RANKL, receptor activator of nuclear factor kappa-B ligand, NSCLC, non-small cell lung cancer, SOD, superoxide dismutase, parasitic diseases, TIMP, tissue inhibitor of metalloproteinases, Ym2, chitinase 3-like protein 4, HNF4A, hepatocyte nuclear factor 4 alpha, Pandemics, Mac, macrophage, Reactive oxygen species, HCMV, human cytomegalovirus, NLRP3, NLR family pyrin domain containing 3, business.industry, Cell growth, SARS-CoV-2, COVID-19, ASC, apoptosis-associated speck-like protein containing CARD, EGFR, epidermal growth factor receptor, AIF, apoptosis-inducing factor, MAPK, mitogen-activated protein kinases, inflammation, Keap1, kelch-like ECH-associated protein 1, Axin2, axis inhibition protein 2, business, sm-α, actin smooth muscle-α actin
Abstract

Graphical abstract Molecular targets modulated by artemisinins in respiratory diseases., Artemisinins are sesquiterpene lactones with a peroxide moiety that are isolated from the herb Artemisia annua. It has been used for centuries for the treatment of fever and chills, and has been recently approved for the treatment of malaria due to its endoperoxidase properties. Progressively, research has found that artemisinins displayed multiple pharmacological actions against inflammation, viral infections, and cell and tumour proliferation, making them effective against diseases. Moreover, it has displayed a relatively safe toxicity profile. The use of artemisinins against different respiratory diseases has been investigated in lung cancer models and inflammatory-driven respiratory disorders. These studies revealed the ability of artemisinins in attenuating proliferation, inflammation, invasion, and metastasis, and in inducing apoptosis. Artemisinins can regulate the expression of pro-inflammatory cytokines, nuclear factor-kappa B (NF-κB), matrix metalloproteinases (MMPs), vascular endothelial growth factor (VEGF), promote cell cycle arrest, drive reactive oxygen species (ROS) production and induce Bak or Bax-dependent or independent apoptosis. In this review, we aim to provide a comprehensive update of the current knowledge of the effects of artemisinins in relation to respiratory diseases to identify gaps that need to be filled in the course of repurposing artemisinins for the treatment of respiratory diseases. In addition, we postulate whether artemisinins can also be repurposed for the treatment of COVID-19 given its anti-viral and anti-inflammatory properties.

Published
2020
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