Pub Date : 2020-12-28DOI: 10.33696/signaling.1.029
Tamara Maiuri, R. Truant
195 N6-fufuryladenine (N6FFA), or kinetin, has a long history as a plant cytokine with practical applications in agriculture. This adenosine analog is now commonplace in natural product small molecule chemical screening libraries, and as such has been discovered as active in mammalian disease pathways that include Parkinson’s disease, Huntington’s disease (HD) and Familial Dysautonomia. We provide a perspective on our data relative to HD and recent discoveries of genetic modifiers of this disease predominantly related to DNA damage repair. We outline the importance of nucleotide salvage and the presence of this adenosine analog in human samples and efficacy in models of human disease, with mechanisms that are empowered by chemical studies using N6FFA as a nucleic acid crosslinking agent.
{"title":"Kinetin/N6-furfuryladenine: A New Neurodegenerative Disease Lead from an Old Plant Cytokine","authors":"Tamara Maiuri, R. Truant","doi":"10.33696/signaling.1.029","DOIUrl":"https://doi.org/10.33696/signaling.1.029","url":null,"abstract":"195 N6-fufuryladenine (N6FFA), or kinetin, has a long history as a plant cytokine with practical applications in agriculture. This adenosine analog is now commonplace in natural product small molecule chemical screening libraries, and as such has been discovered as active in mammalian disease pathways that include Parkinson’s disease, Huntington’s disease (HD) and Familial Dysautonomia. We provide a perspective on our data relative to HD and recent discoveries of genetic modifiers of this disease predominantly related to DNA damage repair. We outline the importance of nucleotide salvage and the presence of this adenosine analog in human samples and efficacy in models of human disease, with mechanisms that are empowered by chemical studies using N6FFA as a nucleic acid crosslinking agent.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"54 1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89333022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.021
Alison Dumont, Steven Lohard, L. Maillet, P. Juin, S. Barillé-Nion
Apoptosis, a programmed cell death relying on the cascade activation of caspases, regulates many processes ranging from embryonic development to immune homeostasis, and plays a major role in cancer. Escape from apoptosis is indeed one of the fundamental characteristics of tumor cells that frequently exhibit increased expression of the main prosurvival BCL-2 homologues BCL-2, BCL-xL and/ or MCL-1 contributing to tumor progression or resistance to anticancer treatments [1]. Mitochondria Outer Membrane Permeabilization (MOMP) is a key cellular event in apoptosis as subsequent release of cytochrome-c (cyto-c) from the mitochondrial intermembrane space to cytosol through BAX/BAK pores, promotes apoptosome formation and downstream activation of apoptotic effector caspases. MOMP can also lead to the release of other mitochondrial components including mitochondrial DNA that engage additional inflammatory signalling pathways inhibited by apoptotic caspases [2,3]. BCL-2 family proteins tightly control BAX/BAK-dependent MOM permeability through a dynamic network of protein-protein interactions integrating various cellular stresses and finally dictating life or death decisions and cell fates [4]. Chemotherapies often upregulate expression of proapoptotic BCL-2 homologues in cancer cells, shifting by this way the balanced death/survival signals towards apoptosis as an expected cytotoxic effect. Among the proapoptotic BH3only proteins of the BCL-2 family, NOXA is unique since in preferentially inhibiting the prosurvival BCL-2 homologue MCL-1, it decreases the protective effect MCL-1 exerts on mitochondrial membranes and transfers MOM integrity surveillance and downstream prevention of caspase activation, mostly to BCL-2 and/or BCL-xL. This was observed in particular during mitotic-related stress after antimitotic treatment or during endoplasmic reticulum (ER) stress induced by proteasome inhibitors, where NOXA was shown to accumulate through transcriptional or post-translational mechanisms, as we detail in this review. Importantly, prosurvival members of BCL-2 family are Abstract
{"title":"NOXA the BCL-2 Family Member behind the Scenes in Cancer Treatment","authors":"Alison Dumont, Steven Lohard, L. Maillet, P. Juin, S. Barillé-Nion","doi":"10.33696/signaling.1.021","DOIUrl":"https://doi.org/10.33696/signaling.1.021","url":null,"abstract":"Apoptosis, a programmed cell death relying on the cascade activation of caspases, regulates many processes ranging from embryonic development to immune homeostasis, and plays a major role in cancer. Escape from apoptosis is indeed one of the fundamental characteristics of tumor cells that frequently exhibit increased expression of the main prosurvival BCL-2 homologues BCL-2, BCL-xL and/ or MCL-1 contributing to tumor progression or resistance to anticancer treatments [1]. Mitochondria Outer Membrane Permeabilization (MOMP) is a key cellular event in apoptosis as subsequent release of cytochrome-c (cyto-c) from the mitochondrial intermembrane space to cytosol through BAX/BAK pores, promotes apoptosome formation and downstream activation of apoptotic effector caspases. MOMP can also lead to the release of other mitochondrial components including mitochondrial DNA that engage additional inflammatory signalling pathways inhibited by apoptotic caspases [2,3]. BCL-2 family proteins tightly control BAX/BAK-dependent MOM permeability through a dynamic network of protein-protein interactions integrating various cellular stresses and finally dictating life or death decisions and cell fates [4]. Chemotherapies often upregulate expression of proapoptotic BCL-2 homologues in cancer cells, shifting by this way the balanced death/survival signals towards apoptosis as an expected cytotoxic effect. Among the proapoptotic BH3only proteins of the BCL-2 family, NOXA is unique since in preferentially inhibiting the prosurvival BCL-2 homologue MCL-1, it decreases the protective effect MCL-1 exerts on mitochondrial membranes and transfers MOM integrity surveillance and downstream prevention of caspase activation, mostly to BCL-2 and/or BCL-xL. This was observed in particular during mitotic-related stress after antimitotic treatment or during endoplasmic reticulum (ER) stress induced by proteasome inhibitors, where NOXA was shown to accumulate through transcriptional or post-translational mechanisms, as we detail in this review. Importantly, prosurvival members of BCL-2 family are Abstract","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"35 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79196870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.022
F. Dequiedt, T. Cherrier
1University of Liège, Interdisciplinary Cluster for Applied Genoproteomics (GIGA), Liège, Belgium 2University of Liège, GIGA-Molecular Biology of Diseases, Liège, Belgium 3University Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-GreffonTumeur/Ingénierie Cellulaire et Génique, Fédération Hospitalo-Universitaire INCREASE, LabEx LipSTIC, F-25000 Besançon, France *Correspondence should be addressed to Thomas CHERRIER; thomas.cherrier@efs.sante.fr
{"title":"Refining the Class IIa HDAC/MEF2 Paradigm in Muscle Biology: More than Meets the Eye","authors":"F. Dequiedt, T. Cherrier","doi":"10.33696/signaling.1.022","DOIUrl":"https://doi.org/10.33696/signaling.1.022","url":null,"abstract":"1University of Liège, Interdisciplinary Cluster for Applied Genoproteomics (GIGA), Liège, Belgium 2University of Liège, GIGA-Molecular Biology of Diseases, Liège, Belgium 3University Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-GreffonTumeur/Ingénierie Cellulaire et Génique, Fédération Hospitalo-Universitaire INCREASE, LabEx LipSTIC, F-25000 Besançon, France *Correspondence should be addressed to Thomas CHERRIER; thomas.cherrier@efs.sante.fr","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73433968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.026
A. Rehman, H. Wan
Desmoglein-3 (Dsg3) belongs to a subfamily of the desmosomal cadherins and is an essential component of the junctional protein complex known as the desmosome that mediates calcium-dependent cell-cell adhesion in vertebrate epithelial cells [1]. Desmosomes occur in abundance in tissues, such as the skin and mucous membrane that are subjected to extensive mechanical stress. In addition to its role in cell-cell adhesion, Dsg3 also functions as a surface regulator for various intracellular signaling pathways in epithelial cells [1-7]. Many of these findings are achieved from the studies of the pathogenesis of Pemphigus Vulgaris (PV), an autoimmune bullous disease in which Dsg3 serves as a major autoantigen and is targeted by circulating autoantibodies that cause disruption of desmosomes, resulting in blistering affecting both the skin and mucous membrane [2,3,6]. This minireview will focus on our recent findings suggesting an unprecedented signaling role of Dsg3 in regulating two fundamental pathways that control cell proliferation and cell fate decision [8,9]. The involvement of this pathway in the pathogenesis of PV is also discussed briefly in this review.
{"title":"A Novel Regulatory Pathway of Desmoglein-3 in Keratinocyte Stress Response","authors":"A. Rehman, H. Wan","doi":"10.33696/signaling.1.026","DOIUrl":"https://doi.org/10.33696/signaling.1.026","url":null,"abstract":"Desmoglein-3 (Dsg3) belongs to a subfamily of the desmosomal cadherins and is an essential component of the junctional protein complex known as the desmosome that mediates calcium-dependent cell-cell adhesion in vertebrate epithelial cells [1]. Desmosomes occur in abundance in tissues, such as the skin and mucous membrane that are subjected to extensive mechanical stress. In addition to its role in cell-cell adhesion, Dsg3 also functions as a surface regulator for various intracellular signaling pathways in epithelial cells [1-7]. Many of these findings are achieved from the studies of the pathogenesis of Pemphigus Vulgaris (PV), an autoimmune bullous disease in which Dsg3 serves as a major autoantigen and is targeted by circulating autoantibodies that cause disruption of desmosomes, resulting in blistering affecting both the skin and mucous membrane [2,3,6]. This minireview will focus on our recent findings suggesting an unprecedented signaling role of Dsg3 in regulating two fundamental pathways that control cell proliferation and cell fate decision [8,9]. The involvement of this pathway in the pathogenesis of PV is also discussed briefly in this review.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76756943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.027
W. Jaross
Endogenous electric and electromagnetic phenomena are increasingly becoming a focus of research in these areas [111]. The vibrations of molecules, molecule parts, molecular aggregates, and cell organelles generate electromagnetic radiation with frequencies in the infrared range at the temperature of life. Although the energy of this radiation is very low, this radiation appears principally suitable for intracellular as well as extracellular signalling processes.
{"title":"The Possible Role of Molecular Vibration in Intracellular Signalling","authors":"W. Jaross","doi":"10.33696/signaling.1.027","DOIUrl":"https://doi.org/10.33696/signaling.1.027","url":null,"abstract":"Endogenous electric and electromagnetic phenomena are increasingly becoming a focus of research in these areas [111]. The vibrations of molecules, molecule parts, molecular aggregates, and cell organelles generate electromagnetic radiation with frequencies in the infrared range at the temperature of life. Although the energy of this radiation is very low, this radiation appears principally suitable for intracellular as well as extracellular signalling processes.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79151779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.028
Dingmei Zhang, Mei Li, Zheng-Hong Qin
1Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China 2Department of Pediatrics Research Institute, Children’s Hospital of Soochow University, Suzhou, 215025, China 3Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
{"title":"The Role of TIGAR-mediated Metabolic Processes in Autophagy and Cell Survival","authors":"Dingmei Zhang, Mei Li, Zheng-Hong Qin","doi":"10.33696/signaling.1.028","DOIUrl":"https://doi.org/10.33696/signaling.1.028","url":null,"abstract":"1Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China 2Department of Pediatrics Research Institute, Children’s Hospital of Soochow University, Suzhou, 215025, China 3Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83197049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-28DOI: 10.33696/signaling.1.023
Ying Li, Bing Liu, D. Reverter
151 Protein ubiquitination is a major post-translational mechanism that regulates fate and function of many proteins in the cell, either by regulating their abundance by the 26S-proteasome-ubiquitin system or by modulating protein activity by the attachment of the ubiquitin modifier [1]. Thus, in addition to targeting proteins for proteasomal degradation, ubiquitin plays a role in many other non-degradative processes in the cell, including transcription, cell cycle, DNA repair, apoptosis, immune response, endosomal sorting, among others [2]. Protein ubiquitination requires the coordination of an enzymatic cascade composed by the E1 activation enzyme, E2 conjugating enzyme, and the E3 ligase. Sometimes, E2 can directly guide ubiquitin to bind to the substrate, but in most circumstances, the cooperative work of E3 ligase is required for catalysis and specificity [3]. Deubiquitinating enzymes (DUBs) can reverse ubiquitination by removing ubiquitin from protein targets having an opposite function to the E3 ligases. Coordination of these two activities contributes to the fine-tune regulation of target ubiquitination inside the cell, and in some cases their abundance or half-life when ubiquitin targets protein degradation by the proteasome. Deregulation of DUBs activity can be linked to several diseases, such as cancer or neurodegeneration among others, indicating the major role of this proteolytic activity for a correct cellular homeostasis.
{"title":"A Novel Regulatory Mechanism to Regulate the Deubiquitinating Activity of USP25 by Oligomerization","authors":"Ying Li, Bing Liu, D. Reverter","doi":"10.33696/signaling.1.023","DOIUrl":"https://doi.org/10.33696/signaling.1.023","url":null,"abstract":"151 Protein ubiquitination is a major post-translational mechanism that regulates fate and function of many proteins in the cell, either by regulating their abundance by the 26S-proteasome-ubiquitin system or by modulating protein activity by the attachment of the ubiquitin modifier [1]. Thus, in addition to targeting proteins for proteasomal degradation, ubiquitin plays a role in many other non-degradative processes in the cell, including transcription, cell cycle, DNA repair, apoptosis, immune response, endosomal sorting, among others [2]. Protein ubiquitination requires the coordination of an enzymatic cascade composed by the E1 activation enzyme, E2 conjugating enzyme, and the E3 ligase. Sometimes, E2 can directly guide ubiquitin to bind to the substrate, but in most circumstances, the cooperative work of E3 ligase is required for catalysis and specificity [3]. Deubiquitinating enzymes (DUBs) can reverse ubiquitination by removing ubiquitin from protein targets having an opposite function to the E3 ligases. Coordination of these two activities contributes to the fine-tune regulation of target ubiquitination inside the cell, and in some cases their abundance or half-life when ubiquitin targets protein degradation by the proteasome. Deregulation of DUBs activity can be linked to several diseases, such as cancer or neurodegeneration among others, indicating the major role of this proteolytic activity for a correct cellular homeostasis.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81493501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-01DOI: 10.33696/Signaling.1.024
W Zhong, N A Darmani
Nausea and vomiting are protective defense mechanisms by which vomit competent species avoid ingestion of potentially toxic substances. More specifically, vomiting is the act of forceful expulsion of gastrointestinal contents through the mouth, whereas nausea is an unpleasant painless subjective feeling that one will imminently vomit. Severe or chronic vomiting can become detrimental due to significant loss of fluid and ion imbalance. The act of vomiting is usually preceded by retching, where the gastrointestinal tract contents are forced into the esophagus, without the vomitus being expelled [1]. While significant knowledge exists on the neurotransmitter and anatomical basis of vomiting [2-4], nausea is the neglected symptom and its anatomical neurochemistry remains to be fully defined.
{"title":"Role of PI3K/Akt/GSK-3 Pathway in Emesis and Potential New Antiemetics.","authors":"W Zhong, N A Darmani","doi":"10.33696/Signaling.1.024","DOIUrl":"https://doi.org/10.33696/Signaling.1.024","url":null,"abstract":"Nausea and vomiting are protective defense mechanisms by which vomit competent species avoid ingestion of potentially toxic substances. More specifically, vomiting is the act of forceful expulsion of gastrointestinal contents through the mouth, whereas nausea is an unpleasant painless subjective feeling that one will imminently vomit. Severe or chronic vomiting can become detrimental due to significant loss of fluid and ion imbalance. The act of vomiting is usually preceded by retching, where the gastrointestinal tract contents are forced into the esophagus, without the vomitus being expelled [1]. While significant knowledge exists on the neurotransmitter and anatomical basis of vomiting [2-4], nausea is the neglected symptom and its anatomical neurochemistry remains to be fully defined.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 4","pages":"155-159"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7793561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39140582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-10-31DOI: 10.33696/signaling.1.025
A. Bennett, A. Lawan
Obesity has reached a global epidemic and it predisposes to the development of insulin resistance, type 2 diabetes and related metabolic diseases. Current interventions against obesity and/or type 2 diabetes such as calorie restriction, exercise, genetic manipulations or established pharmacological treatments have not been successful for many patients with obesity and/or type 2 diabetes. There is an urgent need for new strategies to treat insulin resistance, T2D and obesity. Increased activity of stress-responsive pathways has been linked to the pathogenesis of insulin resistance in obesity. In this commentary, we argue that chronic upregulation of MKP-1 in skeletal muscle is part of a stress response that contributes to the development of insulin resistance, T2D and obesity. Therefore, inhibition of MKP-1 in skeletal muscle is a potential strategy for the treatment of T2D and obesity. We highlight therapeutic strategies for potential targeting of MKP-1 in skeletal muscle for the treatment of metabolic diseases as well as other diseases of skeletal muscle.
{"title":"Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1","authors":"A. Bennett, A. Lawan","doi":"10.33696/signaling.1.025","DOIUrl":"https://doi.org/10.33696/signaling.1.025","url":null,"abstract":"Obesity has reached a global epidemic and it predisposes to the development of insulin resistance, type 2 diabetes and related metabolic diseases. Current interventions against obesity and/or type 2 diabetes such as calorie restriction, exercise, genetic manipulations or established pharmacological treatments have not been successful for many patients with obesity and/or type 2 diabetes. There is an urgent need for new strategies to treat insulin resistance, T2D and obesity. Increased activity of stress-responsive pathways has been linked to the pathogenesis of insulin resistance in obesity. In this commentary, we argue that chronic upregulation of MKP-1 in skeletal muscle is part of a stress response that contributes to the development of insulin resistance, T2D and obesity. Therefore, inhibition of MKP-1 in skeletal muscle is a potential strategy for the treatment of T2D and obesity. We highlight therapeutic strategies for potential targeting of MKP-1 in skeletal muscle for the treatment of metabolic diseases as well as other diseases of skeletal muscle.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"111 1","pages":"160 - 168"},"PeriodicalIF":0.0,"publicationDate":"2020-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73979953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-07DOI: 10.33696/signaling.1.014
F. Armutcu, S. Akyol, Huseyin Vura
Background: Metabolic syndrome (MS) is an important clinical and public health problem, especially in Western society, and is affecting more and more people worldwide. Although most cases of MS are considered obese and insulin-resistant, they are characterized by inflammatory cytokine activity and chronic low-grade inflammation. Also, assumptions about the role of MS and organ interaction during target organ damage become increasingly important. Method: For this study, online research and screening were carried out in electronic databases such as PubMed, Web of Science, and Google Scholar; using the terms “metabolic syndrome” and “organ crosstalk” as keywords. Results: Due to the unpredictable clinical course and treatment uncertainty in this multi-factor chronic disease, increased organ interaction and complications lead to an increase of biomarkers in blood circulation, each of which has diagnostic potential. Therefore, a better understanding of inflammatory triggers and organ interferences will also help determine therapeutic targets and prevent organ damage associated with metabolic syndrome. Conclusion: This mini review presents an overview of the relationship between MS and organ crosstalk. More research is needed to fully elucidate the relationship between MS and organ crosstalk, the pathological conditions it causes, and biomarkers related to MS.
背景:代谢综合征(MS)是一个重要的临床和公共卫生问题，特别是在西方社会，并影响着越来越多的人。虽然大多数MS病例被认为是肥胖和胰岛素抵抗，但它们的特征是炎症细胞因子活性和慢性低度炎症。此外，在靶器官损伤过程中，关于MS和器官相互作用的假设也变得越来越重要。方法:本研究在PubMed、Web of Science、Google Scholar等电子数据库中进行在线研究和筛选;以“代谢综合征”和“器官相声”为关键词。结果:由于这种多因素慢性疾病的临床病程和治疗不确定性，器官相互作用和并发症的增加导致血液循环中生物标志物的增加，每种生物标志物都具有诊断潜力。因此，更好地了解炎症触发因素和器官干扰也将有助于确定治疗靶点和预防代谢综合征相关的器官损伤。结论:本文综述了MS与器官串扰的关系。需要更多的研究来充分阐明MS与器官串扰的关系、其引起的病理状况以及与MS相关的生物标志物。
{"title":"Metabolic Syndrome is an Important Cornerstone in the Health-disease Line and Pathological Organ Interaction","authors":"F. Armutcu, S. Akyol, Huseyin Vura","doi":"10.33696/signaling.1.014","DOIUrl":"https://doi.org/10.33696/signaling.1.014","url":null,"abstract":"Background: Metabolic syndrome (MS) is an important clinical and public health problem, especially in Western society, and is affecting more and more people worldwide. Although most cases of MS are considered obese and insulin-resistant, they are characterized by inflammatory cytokine activity and chronic low-grade inflammation. Also, assumptions about the role of MS and organ interaction during target organ damage become increasingly important. Method: For this study, online research and screening were carried out in electronic databases such as PubMed, Web of Science, and Google Scholar; using the terms “metabolic syndrome” and “organ crosstalk” as keywords. Results: Due to the unpredictable clinical course and treatment uncertainty in this multi-factor chronic disease, increased organ interaction and complications lead to an increase of biomarkers in blood circulation, each of which has diagnostic potential. Therefore, a better understanding of inflammatory triggers and organ interferences will also help determine therapeutic targets and prevent organ damage associated with metabolic syndrome. Conclusion: This mini review presents an overview of the relationship between MS and organ crosstalk. More research is needed to fully elucidate the relationship between MS and organ crosstalk, the pathological conditions it causes, and biomarkers related to MS.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"47 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81685772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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