PPAR Research最新文献

{"title":"Fenofibrate Protects Cardiomyocytes from Hypoxia/Reperfusion- and High Glucose-Induced Detrimental Effects.","authors":"Fabiola Cortes-Lopez,&nbsp;Alicia Sanchez-Mendoza,&nbsp;David Centurion,&nbsp;Luz G Cervantes-Perez,&nbsp;Vicente Castrejon-Tellez,&nbsp;Leonardo Del Valle-Mondragon,&nbsp;Elizabeth Soria-Castro,&nbsp;Victoria Ramirez,&nbsp;Araceli Sanchez-Lopez,&nbsp;Gustavo Pastelin-Hernandez,&nbsp;Wylly Ramses Garcia-Niño,&nbsp;Maria Sanchez-Aguilar,&nbsp;Luz Ibarra-Lara","doi":"10.1155/2021/8895376","DOIUrl":"https://doi.org/10.1155/2021/8895376","url":null,"abstract":"<p><p>Lesions caused by high glucose (HG), hypoxia/reperfusion (H/R), and the coexistence of both conditions in cardiomyocytes are linked to an overproduction of reactive oxygen species (ROS), causing irreversible damage to macromolecules in the cardiomyocyte as well as its ultrastructure. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR<i>α</i>) agonist, promotes beneficial activities counteracting cardiac injury. Therefore, the objective of this work was to determine the potential protective effect of fenofibrate in cardiomyocytes exposed to HG, H/R, and HG+H/R. Cardiomyocyte cultures were divided into four main groups: (1) control (CT), (2) HG (25 mM), (3) H/R, and (4) HG+H/R. Our results indicate that cell viability decreases in cardiomyocytes undergoing HG, H/R, and both conditions, while fenofibrate improves cell viability in every case. Fenofibrate also decreases ROS production as well as nicotinamide adenine dinucleotide phosphate oxidase (NADPH) subunit expression. Regarding the antioxidant defense, superoxide dismutase (SOD Cu²⁺/Zn²⁺ and SOD Mn²⁺), catalase, and the antioxidant capacity were decreased in HG, H/R, and HG+H/R-exposed cardiomyocytes, while fenofibrate increased those parameters. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) increased significantly in treated cells, while pathologies increased the expression of its inhibitor Keap1. Oxidative stress-induced mitochondrial damage was lower in fenofibrate-exposed cardiomyocytes. Endothelial nitric oxide synthase was also favored in cardiomyocytes treated with fenofibrate. Our results suggest that fenofibrate preserves the antioxidant status and the ultrastructure in cardiomyocytes undergoing HG, H/R, and HG+H/R preventing damage to essential macromolecules involved in the proper functioning of the cardiomyocyte.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"8895376"},"PeriodicalIF":2.9,"publicationDate":"2021-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7811426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38869217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant Potential of Adiponectin and Full PPAR-<i>γ</i> Agonist in Correcting Streptozotocin-Induced Vascular Abnormality in Spontaneously Hypertensive Rats.","authors":"Sheryar Afzal,&nbsp;Munavvar Abdul Sattar,&nbsp;Edward James Johns,&nbsp;Olorunfemi A Eseyin,&nbsp;Ali Attiq","doi":"10.1155/2021/6661181","DOIUrl":"https://doi.org/10.1155/2021/6661181","url":null,"abstract":"<p><p>Oxidative stress, which is associated with metabolic and anthropometric perturbations, leads to reactive oxygen species production and decrease in plasma adiponectin concentration. We investigated pharmacodynamically the pathophysiological role and potential implication of exogenously administered adiponectin with full and partial peroxisome proliferator-activated receptor-gamma (PPAR-<i>γ</i>) agonists on modulation of oxidative stress, metabolic dysregulation, and antioxidant potential in streptozotocin-induced spontaneously hypertensive rats (SHR). Group I (WKY) serves as the normotensive control, whereas 42 male SHRs were randomized equally into 7 groups (<i>n</i> = 6); group II serves as the SHR control, group III serves as the SHR diabetic control, and groups IV, V, and VI are treated with irbesartan (30 mg/kg), pioglitazone (10 mg/kg), and adiponectin (2.5 <i>μ</i>g/kg), whereas groups VII and VIII received cotreatments as irbesartan+adiponectin and pioglitazone+adiponectin, respectively. Diabetes was induced using an intraperitoneal injection of streptozotocin (40 mg/kg). Plasma adiponectin, lipid contents, and arterial stiffness with oxidative stress biomarkers were measured using an in vitro and in vivo analysis. Diabetic SHRs exhibited hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and increased arterial stiffness with reduced plasma adiponectin and antioxidant enzymatic levels (<i>P</i> < 0.05). Diabetic SHRs pretreated with pioglitazone and adiponectin separately exerted improvements in antioxidant enzyme activities, abrogated arterial stiffness, and offset the increased production of reactive oxygen species and dyslipidemic effects of STZ, whereas the blood pressure values were significantly reduced in the irbesartan-treated groups (all <i>P</i> < 0.05). The combined treatment of exogenously administered adiponectin with full PPAR-<i>γ</i> agonist augmented the improvement in lipid contents and adiponectin concentration and restored arterial stiffness with antioxidant potential effects, indicating the degree of synergism between adiponectin and full PPAR-<i>γ</i> agonists (pioglitazone).</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2021 ","pages":"6661181"},"PeriodicalIF":2.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8531825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10697748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bergenin Attenuates Hepatic Fibrosis by Regulating Autophagy Mediated by the PPAR-<i>γ</i>/TGF-<i>β</i> Pathway.","authors":"Yujing Xia,&nbsp;Jingjing Li,&nbsp;Kan Chen,&nbsp;Jiao Feng,&nbsp;Chuanyong Guo","doi":"10.1155/2020/6694214","DOIUrl":"https://doi.org/10.1155/2020/6694214","url":null,"abstract":"<p><p>Liver fibrosis is a pathological process involving diffuse extracellular matrix (ECM) deposition in the liver. It is typical of many chronic liver diseases, including cirrhosis, and effective drugs are needed. In this study, we explored the protective effect of bergenin on liver fibrosis induced by carbon tetrachloride and bile duct ligation. A variety of molecular biological methods (qRT-PCR, western blotting, and immunohistochemistry) were employed to confirm the increased degree of hepatocyte injury and ECM formation in the disease model, consistent with autophagy and activation of the TGF-<i>β</i> pathway. Bergenin activated PPAR-<i>γ</i> and inhibited TGF-<i>β</i> and autophagy and decreased liver fibrosis by inhibiting hepatocyte necrosis and ECM formation in a dose-dependent manner. The results suggest that bergenin may be a promising drug candidate for the treatment of liver fibrosis.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"6694214"},"PeriodicalIF":2.9,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7790590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38854144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ligand-Activated Peroxisome Proliferator-Activated Receptor <i>β</i>/<i>δ</i> Facilitates Cell Proliferation in Human Cholesteatoma Keratinocytes.","authors":"Chen Zhang,&nbsp;Yang-Wenyi Liu,&nbsp;Zhangcai Chi,&nbsp;Bing Chen","doi":"10.1155/2020/8864813","DOIUrl":"https://doi.org/10.1155/2020/8864813","url":null,"abstract":"<p><p>Cholesteatoma is characterized by both the overgrowth of hyperkeratinized squamous epithelium and bone erosion. However, the exact mechanism underlying the hyperproliferative ability of cholesteatoma remains unknown. In this study, we investigated PPAR <i>β</i>/<i>δ</i> expression in human surgical specimens of cholesteatoma and analyzed its functional role as a regulator of epithelial keratinocyte hyperproliferation. We found that the expression of PPAR <i>β</i>/<i>δ</i> was significantly upregulated in cholesteatoma and ligand-activated PPAR <i>β</i>/<i>δ</i> markedly promoted the proliferation of cholesteatoma keratinocytes. Furthermore, we showed that PPAR <i>β</i>/<i>δ</i> activation increased PDK1 expression and decreased PTEN generation, which led to increased phosphorylation of AKT and GSK3<i>β</i> and increased the expression level of Cyclin D1. Overall, our data suggested that the proliferating effect of PPAR <i>β</i>/<i>δ</i> on the cholesteatoma keratinocytes was mediated by the positive regulation of the PDK1/PTEN/AKT/GSK3<i>β</i>/Cyclin D1 pathway. These findings warranted further investigation of PPAR <i>β</i>/<i>δ</i> as a therapeutic target for recurrent or residual cholesteatoma.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"8864813"},"PeriodicalIF":2.9,"publicationDate":"2020-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7781706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38804542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-21 Contributes to Acute Liver Injury in LPS-Induced Sepsis Mice by Inhibiting PPAR<i>α</i> Expression.","authors":"Xianjin Du,&nbsp;Miao Wu,&nbsp;Dan Tian,&nbsp;Jianlin Zhou,&nbsp;Lu Wang,&nbsp;Liying Zhan","doi":"10.1155/2020/6633022","DOIUrl":"https://doi.org/10.1155/2020/6633022","url":null,"abstract":"<p><p>The severity of sepsis may be associated with excessive inflammation, thus leading to acute liver injury. MicroRNA-21 is highly expressed in the liver of a variety of inflammation-related diseases, and PPAR<i>α</i> is also proved to participate in regulating inflammation. In the present study, the LPS-induced sepsis model was established. We found that microRNA-21 expression was upregulated in the liver of sepsis mice, and microRNA-21 inhibition significantly reduced the liver injury. The expression of liver injury markers, inflammation cytokines, and PPAR<i>α</i> in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPAR<i>α</i> is the target gene of microRNA-21; PPAR<i>α</i> antagonist GW6471 could reverse the effect of antagomir-21. In conclusion, our study illustrated that microRNA-21 exacerbate acute liver injury in sepsis mice by inhibiting PPAR<i>α</i> expression.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"6633022"},"PeriodicalIF":2.9,"publicationDate":"2020-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7772039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38804541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPAR<i>α</i> Agonist WY-14643 Relieves Neuropathic Pain through SIRT1-Mediated Deacetylation of NF-<i>κ</i>B.","authors":"Wanshun Wen,&nbsp;Jinlin Wang,&nbsp;Biyu Zhang,&nbsp;Jun Wang","doi":"10.1155/2020/6661642","DOIUrl":"https://doi.org/10.1155/2020/6661642","url":null,"abstract":"<p><p>Inflammation caused by neuropathy contributes to the development of neuropathic pain (NP), but the exact mechanism still needs to be understood. Peroxisome proliferator-activated receptor <i>α</i> (PPAR<i>α</i>), an important inflammation regulator, might participate in the inflammation in NP. To explore the role of PPAR<i>α</i> in NP, the effects of PPAR<i>α</i> agonist WY-14643 on chronic constriction injury (CCI) rats were evaluated. The results showed that WY-14643 stimulation could decrease inflammation and relieve neuropathic pain, which was relative with the activation of PPAR<i>α</i>. In addition, we also found that the SIRT1/NF-<i>κ</i>B pathway was involved in the WY-14643-induced anti-inflammation in NP, and activation of PPAR<i>α</i> increased SIRT1 expression, thus reducing the proinflammatory function of NF-<i>κ</i>B. These data suggested that WY-14643 might serve as an inflammation mediator, which may be a potential therapy option for NP.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"6661642"},"PeriodicalIF":2.9,"publicationDate":"2020-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/6661642","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38794143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction.","authors":"Olga I Rudko,&nbsp;Artemii V Tretiakov,&nbsp;Elena A Naumova,&nbsp;Eugene A Klimov","doi":"10.1155/2020/8859017","DOIUrl":"https://doi.org/10.1155/2020/8859017","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptor (PPAR) group includes three isoforms encoded by PPARG, PPARA, and PPARD genes. High concentrations of PPARs are found in parts of the brain linked to anxiety development, including hippocampus and amygdala. Among three PPAR isoforms, PPARG demonstrates the highest expression in CNS, where it can be found in neurons, astrocytes, and glial cells. Herein, the highest PPARG expression occurs in amygdala. However, little is known considering possible connections between PPARs and anxiety behavior. We reviewed possible connections between PPARs and anxiety. We used the Pathway Studio software (Elsevier). Signal pathways were created according to previously developed algorithms. SNEA was performed in Pathway Studio. Current study revealed 14 PPAR-regulated proteins linked to anxiety. Possible mechanism of PPAR involvement in neuroinflammation protection is proposed. Signal pathway reconstruction and reviewing aimed to reveal possible connection between PPARG and CCK-ergic system was conducted. Said analysis revealed that PPARG-dependent regulation of MME and ACE peptidase expression may affect levels of nonhydrolysed, i.e., active CCK-4. Impairments in PPARG regulation and following MME and ACE peptidase expression impairments in amygdala may be the possible mechanism leading to pathological anxiety development, with brain CCK-4 accumulation being a key link. Literature data analysis and signal pathway reconstruction and reviewing revealed two possible mechanisms of peroxisome proliferator-activated receptors involvement in pathological anxiety: (1) cytokine expression and neuroinflammation mechanism and (2) regulation of peptidases targeted to anxiety-associated neuropeptides, primarily CCK-4, mechanism.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"8859017"},"PeriodicalIF":2.9,"publicationDate":"2020-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8859017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38366716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model.","authors":"María Sánchez-Aguilar,&nbsp;Luz Ibarra-Lara,&nbsp;Leonardo Del Valle-Mondragón,&nbsp;Elizabeth Soria-Castro,&nbsp;Juan Carlos Torres-Narváez,&nbsp;Elizabeth Carreón-Torres,&nbsp;Alicia Sánchez-Mendoza,&nbsp;María Esther Rubio-Ruíz","doi":"10.1155/2020/8894525","DOIUrl":"https://doi.org/10.1155/2020/8894525","url":null,"abstract":"<p><p>The activation of the renin-angiotensin system (RAS) participates in the development of metabolic syndrome (MetS) and in heart failure. PPAR-alpha activation by fenofibrate reverts some of the effects caused by these pathologies. Recently, nonclassical RAS components have been implicated in the pathogenesis of hypertension and myocardial dysfunction; however, their cardiac functions are still controversial. We evaluated if the nonclassical RAS signaling pathways, directed by angiotensin III and angiotensin-(1-7), are involved in the cardioprotective effect of fenofibrate during ischemia in MetS rats. Control (CT) and MetS rats were divided into the following groups: (a) sham, (b) vehicle-treated myocardial infarction (MI-V), and (c) fenofibrate-treated myocardial infarction (MI-F). Angiotensin III and angiotensin IV levels and insulin increased the aminopeptidase (IRAP) expression and decreased the angiotensin-converting enzyme 2 (ACE2) expression in the hearts from MetS rats. Ischemia activated the angiotensin-converting enzyme (ACE)/angiotensin II/angiotensin receptor 1 (AT1R) and angiotensin III/angiotensin IV/angiotensin receptor 4 (AT4R)-IRAP axes. Fenofibrate treatment prevented the damage due to ischemia in MetS rats by favoring the angiotensin-(1-7)/angiotensin receptor 2 (AT2R) axis and inhibiting the angiotensin III/angiotensin IV/AT4R-IRAP signaling pathway. Additionally, fenofibrate downregulated neprilysin expression and increased bradykinin production. These effects of PPAR-alpha activation were accompanied by a reduction in the size of the myocardial infarct and in the activity of serum creatine kinase. Thus, the regulation of the nonclassical axis of RAS forms part of a novel protective effect of fenofibrate in myocardial ischemia.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"8894525"},"PeriodicalIF":2.9,"publicationDate":"2020-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8894525","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38743986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPAR<i>γ</i>/eNOS Signaling Pathway.","authors":"Hua Guo,&nbsp;Qinglan Zhang,&nbsp;Haipo Yuan,&nbsp;Lin Zhou,&nbsp;Fang-Fang Li,&nbsp;Sheng-Ming Wang,&nbsp;Gang Shi,&nbsp;Maojuan Wang","doi":"10.1155/2020/8889612","DOIUrl":"https://doi.org/10.1155/2020/8889612","url":null,"abstract":"<p><p>Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPAR<i>γ</i>, eNOS, C-reactive protein, heptoglobin, IL-1<i>β</i>, TNF-<i>α</i>, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPAR<i>γ</i>. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPAR<i>γ</i>/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"8889612"},"PeriodicalIF":2.9,"publicationDate":"2020-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8889612","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38352121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Model of <i>PPARγ</i>-Downregulated Signaling in Psoriasis.","authors":"Vladimir Sobolev,&nbsp;Anastasia Nesterova,&nbsp;Anna Soboleva,&nbsp;Evgenia Dvoriankova,&nbsp;Anastas Piruzyan,&nbsp;Dzerassa Mildzikhova,&nbsp;Irina Korsunskaya,&nbsp;Oxana Svitich","doi":"10.1155/2020/6529057","DOIUrl":"https://doi.org/10.1155/2020/6529057","url":null,"abstract":"<p><p>Interactions of genes in intersecting signaling pathways, as well as environmental influences, are required for the development of psoriasis. Peroxisome proliferator-activated receptor gamma (<i>PPARγ</i>) is a nuclear receptor and transcription factor which inhibits the expression of many proinflammatory genes. We tested the hypothesis that low levels of <i>PPARγ</i> expression promote the development of psoriatic lesions. We combined experimental results and network functional analysis to reconstruct the model of <i>PPARγ</i>-downregulated signaling in psoriasis. We hypothesize that the expression of <i>IL17</i>, <i>STAT3</i>, <i>FOXP3</i>, and <i>RORC</i> and <i>FOSL1</i> genes in psoriatic skin is correlated with the level of <i>PPARγ</i> expression, and they belong to the same signaling pathway that regulates the development of psoriasis lesion.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"6529057"},"PeriodicalIF":2.9,"publicationDate":"2020-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/6529057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38657491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}