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Bergenin Attenuates Hepatic Fibrosis by Regulating Autophagy Mediated by the PPAR-γ/TGF-β Pathway. 卑尔根素通过调节PPAR-γ/TGF-β途径介导的自噬减轻肝纤维化。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-12-31 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6694214
Yujing Xia, Jingjing Li, Kan Chen, Jiao Feng, Chuanyong Guo

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-β pathway. Bergenin activated PPAR-γ and inhibited TGF-β 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.

肝纤维化是肝脏弥漫性细胞外基质(ECM)沉积的病理过程。它是包括肝硬化在内的许多慢性肝病的典型症状,需要有效的药物治疗。本研究探讨了菜根素对四氯化碳及胆管结扎所致肝纤维化的保护作用。多种分子生物学方法(qRT-PCR、western blotting、免疫组织化学)证实疾病模型中肝细胞损伤程度和ECM形成程度增加,与自噬和TGF-β通路激活一致。甜菜根素通过抑制肝细胞坏死和ECM形成,激活PPAR-γ,抑制TGF-β和自噬,减少肝纤维化,呈剂量依赖性。结果表明,卑尔根素可能是治疗肝纤维化的有希望的候选药物。
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引用次数: 20
Ligand-Activated Peroxisome Proliferator-Activated Receptor β/δ Facilitates Cell Proliferation in Human Cholesteatoma Keratinocytes. 配体活化过氧化物酶体增殖物活化受体β/δ促进人胆脂瘤角质形成细胞的增殖。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-12-22 eCollection Date: 2020-01-01 DOI: 10.1155/2020/8864813
Chen Zhang, Yang-Wenyi Liu, Zhangcai Chi, Bing Chen

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 β/δ 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 β/δ was significantly upregulated in cholesteatoma and ligand-activated PPAR β/δ markedly promoted the proliferation of cholesteatoma keratinocytes. Furthermore, we showed that PPAR β/δ activation increased PDK1 expression and decreased PTEN generation, which led to increased phosphorylation of AKT and GSK3β and increased the expression level of Cyclin D1. Overall, our data suggested that the proliferating effect of PPAR β/δ on the cholesteatoma keratinocytes was mediated by the positive regulation of the PDK1/PTEN/AKT/GSK3β/Cyclin D1 pathway. These findings warranted further investigation of PPAR β/δ as a therapeutic target for recurrent or residual cholesteatoma.

胆脂瘤的特征是角化过度的鳞状上皮过度生长和骨侵蚀。然而,胆脂瘤高增殖能力的确切机制尚不清楚。在这项研究中,我们研究了PPAR β/δ在人胆脂瘤手术标本中的表达,并分析了其作为上皮角质细胞过度增殖的调节因子的功能作用。我们发现PPAR β/δ在胆脂瘤中的表达显著上调,配体激活的PPAR β/δ显著促进了胆脂瘤角质形成细胞的增殖。此外,我们发现PPAR β/δ激活增加了PDK1的表达,减少了PTEN的产生,从而导致AKT和GSK3β磷酸化增加,Cyclin D1表达水平升高。总之,我们的数据表明PPAR β/δ对胆脂瘤角质形成细胞的增殖作用是通过PDK1/PTEN/AKT/GSK3β/Cyclin D1通路的正调控介导的。这些发现为进一步研究PPAR β/δ作为复发性或残留胆脂瘤的治疗靶点提供了依据。
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引用次数: 3
MicroRNA-21 Contributes to Acute Liver Injury in LPS-Induced Sepsis Mice by Inhibiting PPARα Expression. MicroRNA-21通过抑制PPARα表达参与lps诱导的脓毒症小鼠急性肝损伤
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-12-22 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6633022
Xianjin Du, Miao Wu, Dan Tian, Jianlin Zhou, Lu Wang, Liying Zhan

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 PPARα 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 PPARα in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPARα is the target gene of microRNA-21; PPARα 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 PPARα expression.

脓毒症的严重程度可能与过度炎症有关,从而导致急性肝损伤。MicroRNA-21在多种炎症相关疾病的肝脏中高表达,PPARα也被证明参与调节炎症。本研究建立lps致脓毒症模型。我们发现microRNA-21在脓毒症小鼠肝脏中表达上调,抑制microRNA-21可显著减轻肝损伤。脓毒症小鼠的肝损伤标志物、炎症细胞因子和PPARα的表达高于阿塔戈米尔-21处理的脓毒症小鼠。此外,我们还发现PPARα是microRNA-21的靶基因;PPARα拮抗剂GW6471可逆转安他哥米-21的作用。总之,我们的研究表明,microRNA-21通过抑制PPARα的表达加重脓毒症小鼠的急性肝损伤。
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引用次数: 5
PPARα Agonist WY-14643 Relieves Neuropathic Pain through SIRT1-Mediated Deacetylation of NF-κB. PPARα激动剂WY-14643通过sirt1介导的NF-κB去乙酰化缓解神经性疼痛。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-12-14 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6661642
Wanshun Wen, Jinlin Wang, Biyu Zhang, Jun Wang

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 α (PPARα), an important inflammation regulator, might participate in the inflammation in NP. To explore the role of PPARα in NP, the effects of PPARα 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 PPARα. In addition, we also found that the SIRT1/NF-κB pathway was involved in the WY-14643-induced anti-inflammation in NP, and activation of PPARα increased SIRT1 expression, thus reducing the proinflammatory function of NF-κB. These data suggested that WY-14643 might serve as an inflammation mediator, which may be a potential therapy option for NP.

神经病变引起的炎症有助于神经性疼痛(NP)的发展,但其确切机制尚不清楚。过氧化物酶体增殖物激活受体α (PPARα)是一种重要的炎症调节剂,可能参与NP的炎症反应。为了探讨ppara α在NP中的作用,我们观察了ppara α激动剂WY-14643对慢性收缩性损伤(CCI)大鼠的作用。结果表明,WY-14643刺激能减轻炎症反应,减轻神经性疼痛,其作用与PPARα的激活有关。此外,我们还发现SIRT1/NF-κB通路参与wy -14643诱导的NP抗炎,激活PPARα增加SIRT1表达,从而降低NF-κB的促炎功能。这些数据提示WY-14643可能作为炎症介质,可能是NP的潜在治疗选择。
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引用次数: 5
Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction. ppar在焦虑进展中的作用:文献分析和信号通路重建。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-11-29 eCollection Date: 2020-01-01 DOI: 10.1155/2020/8859017
Olga I Rudko, Artemii V Tretiakov, Elena A Naumova, Eugene A Klimov

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.

过氧化物酶体增殖物激活受体(PPAR)组包括由PPARG、PPARA和PPARD基因编码的三种亚型。在大脑中与焦虑发展有关的部分,包括海马体和杏仁核,发现了高浓度的ppar。在三种PPAR亚型中,PPARG在中枢神经系统中表达最高,在神经元、星形胶质细胞和胶质细胞中均有表达。其中,PPARG在杏仁核中表达最高。然而,考虑到ppar和焦虑行为之间的可能联系,我们所知甚少。我们回顾了ppar和焦虑之间可能存在的联系。我们使用了Pathway Studio软件(Elsevier)。信号通路是根据先前开发的算法创建的。SNEA在Pathway Studio进行。目前的研究揭示了14种ppar调节的蛋白质与焦虑有关。提出PPAR参与神经炎症保护的可能机制。为了揭示PPARG与CCK-ergic系统之间可能存在的联系,对信号通路进行了重构和回顾。上述分析显示,pparg依赖性MME和ACE肽酶表达的调控可能影响非水解的,即活性CCK-4的水平。PPARG调控的损伤以及随之而来的杏仁核MME和ACE肽酶表达的损伤可能是导致病理性焦虑发展的可能机制,而脑CCK-4积累是一个关键环节。文献资料分析和信号通路重构与回顾揭示了过氧化物酶体增殖物激活受体参与病理性焦虑的可能机制:(1)细胞因子表达和神经炎症机制;(2)焦虑相关神经肽靶向肽酶调控机制,主要是CCK-4机制。
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引用次数: 4
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. 肾素-血管紧张素系统的非经典轴和Neprilysin:代谢综合征模型中心肌缺血时ppar - α激活的心脏保护作用的关键介质。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-11-27 eCollection Date: 2020-01-01 DOI: 10.1155/2020/8894525
María Sánchez-Aguilar, Luz Ibarra-Lara, Leonardo Del Valle-Mondragón, Elizabeth Soria-Castro, Juan Carlos Torres-Narváez, Elizabeth Carreón-Torres, Alicia Sánchez-Mendoza, María Esther Rubio-Ruíz

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.

肾素-血管紧张素系统(RAS)的激活参与代谢综合征(MetS)和心力衰竭的发展。非诺贝特激活ppar - α可以逆转由这些病理引起的一些影响。最近,非经典RAS成分被认为与高血压和心肌功能障碍的发病机制有关;然而,它们的心脏功能仍然存在争议。我们评估了由血管紧张素III和血管紧张素-(1-7)引导的非经典RAS信号通路是否参与了非诺贝特在MetS大鼠缺血期间的心脏保护作用。对照(CT)和MetS大鼠分为以下组:(a)假手术组,(b)载药治疗的心肌梗死(MI-V)组,(c)非诺贝特治疗的心肌梗死(MI-F)组。血管紧张素III和血管紧张素IV水平和胰岛素增加了氨肽酶(IRAP)的表达,降低了血管紧张素转换酶2 (ACE2)的表达。缺血激活血管紧张素转换酶(ACE)/血管紧张素II/血管紧张素受体1 (AT1R)和血管紧张素III/血管紧张素IV/血管紧张素受体4 (AT4R)-IRAP轴。非诺贝特治疗通过促进血管紧张素-(1-7)/血管紧张素受体2 (AT2R)轴和抑制血管紧张素III/血管紧张素IV/AT4R-IRAP信号通路来预防MetS大鼠缺血损伤。此外,非诺贝特下调了neprilysin的表达,增加了缓激肽的产生。ppar - α活化的这些作用伴随着心肌梗死面积的减小和血清肌酸激酶活性的降低。因此,非诺贝特在心肌缺血中的新保护作用的一部分是对RAS非经典轴的调节。
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引用次数: 2
Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway. 一氧化氮通过PPARγ/eNOS信号通路介导II型糖尿病炎症
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-11-26 eCollection Date: 2020-01-01 DOI: 10.1155/2020/8889612
Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-Fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang

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-1β, TNF-α, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPARγ, eNOS, C-reactive protein, heptoglobin, IL-1β, TNF-α, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPARγ. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPARγ/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.

炎症参与了2型糖尿病(T2DM)的发病过程,其具体机制尚不清楚。一氧化氮(NO)是一种关键的炎症调节剂,其作用是T2DM的炎症,但很少报道。因此,我们的研究旨在探讨NO对T2DM炎症的影响及其机制。采用一氧化氮分析仪分析T2DM患者和配对健康成人血浆样品中的NO水平,测定NO供体或NO清除剂处理胰岛素诱导HepG2细胞中炎症因子(c反应蛋白、肝球蛋白、IL-1β、TNF-α、IL-6)的表达,并采用RT-PCR和western blot检测si-PPARγ转染胰岛素诱导HepG2细胞中PPARγ、eNOS、c反应蛋白、肝球蛋白、IL-1β、TNF-α和IL-6的水平。结果表明,过量NO可增加T2DM患者炎症标志物水平,这是由PPARγ/eNOS通路激活的。这些发现将加强对NO在T2DM中的认识,并为T2DM的治疗提供新的靶点。
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引用次数: 11
The Model of PPARγ-Downregulated Signaling in Psoriasis. 银屑病ppar γ-下调信号通路模型的研究。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-10-09 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6529057
Vladimir Sobolev, Anastasia Nesterova, Anna Soboleva, Evgenia Dvoriankova, Anastas Piruzyan, Dzerassa Mildzikhova, Irina Korsunskaya, Oxana Svitich

Interactions of genes in intersecting signaling pathways, as well as environmental influences, are required for the development of psoriasis. Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor and transcription factor which inhibits the expression of many proinflammatory genes. We tested the hypothesis that low levels of PPARγ expression promote the development of psoriatic lesions. We combined experimental results and network functional analysis to reconstruct the model of PPARγ-downregulated signaling in psoriasis. We hypothesize that the expression of IL17, STAT3, FOXP3, and RORC and FOSL1 genes in psoriatic skin is correlated with the level of PPARγ expression, and they belong to the same signaling pathway that regulates the development of psoriasis lesion.

交叉信号通路中基因的相互作用,以及环境的影响,是银屑病发展所必需的。过氧化物酶体增殖物激活受体γ (PPARγ)是一种核受体和转录因子,可抑制许多促炎基因的表达。我们验证了低水平PPARγ表达促进银屑病病变发展的假设。我们将实验结果与网络功能分析相结合,重建银屑病中ppar γ下调信号通路的模型。我们推测银屑病皮肤中IL17、STAT3、FOXP3、RORC和FOSL1基因的表达与PPARγ表达水平相关,它们属于调节银屑病病变发展的同一信号通路。
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引用次数: 9
The Role of Peroxisome Proliferator-Activated Receptors (PPARs) in Pan-Cancer. 过氧化物酶体增殖物激活受体(PPARs)在泛癌中的作用。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-09-22 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6527564
Runzhi Huang, Jiaqi Zhang, Mingxiao Li, Penghui Yan, Huabin Yin, Suna Zhai, Xiaolong Zhu, Peng Hu, Jiaxin Zhang, Ling Huang, Man Li, Zehui Sun, Tong Meng, Daoke Yang, Zongqiang Huang

Peroxisome proliferator-activated receptors (PPARs) are members of nuclear transcription factors. The functions of the PPAR family (PPARA, PPARD, and PPARG) and their coactivators (PPARGC1A and PPARGC1B) in maintenance of lipid and glucose homeostasis have been unveiled. However, the roles of PPARs in cancer development remain elusive. In this work, we made use of 11,057 samples across 33 TCGA tumor types to analyze the relationship between PPAR transcriptional expression and tumorigenesis as well as drug sensitivity. We performed multidimensional analyses on PPARA, PPARG, PPARD, PPARGC1A, and PPARGC1B, including differential expression analysis in pan-cancer, immune subtype analysis, clinical analysis, tumor purity analysis, stemness correlation analysis, and drug responses. PPARs and their coactivators expressed differently in different types of cancers, in different immune subtypes. This analysis reveals various expression patterns of the PPAR family at a level of pan-cancer and provides new clues for the therapeutic strategies of cancer.

过氧化物酶体增殖体激活受体(PPARs)是核转录因子的成员。PPAR家族(PPARA、PPARD和PPARG)及其共激活物(PPARGC1A和PPARGC1B)在维持脂质和葡萄糖稳态中的功能已经被揭示。然而,ppar在癌症发展中的作用仍然难以捉摸。在这项工作中,我们利用33种TCGA肿瘤类型的11057个样本来分析PPAR转录表达与肿瘤发生以及药物敏感性之间的关系。我们对PPARA、PPARG、PPARD、PPARGC1A和PPARGC1B进行了多维度分析,包括泛癌差异表达分析、免疫亚型分析、临床分析、肿瘤纯度分析、干细胞相关性分析和药物反应分析。ppar及其共激活因子在不同类型的癌症和不同的免疫亚型中表达不同。该分析揭示了PPAR家族在泛癌水平上的多种表达模式,为癌症的治疗策略提供了新的线索。
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引用次数: 12
A New Prognostic Risk Model Based on PPAR Pathway-Related Genes in Kidney Renal Clear Cell Carcinoma. 基于肾脏肾透明细胞癌 PPAR 通路相关基因的新型预后风险模型
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2020-09-22 eCollection Date: 2020-01-01 DOI: 10.1155/2020/6937475
Yingkun Xu, Xiunan Li, Yuqing Han, Zilong Wang, Chenglin Han, Ningke Ruan, Jianyi Li, Xiao Yu, Qinghua Xia, Guangzhen Wu

Objective: This study is aimed at using genes related to the peroxisome proliferator-activated receptor (PPAR) pathway to establish a prognostic risk model in kidney renal clear cell carcinoma (KIRC).

Methods: For this study, we first found the PPAR pathway-related genes on the gene set enrichment analysis (GSEA) website and found the KIRC mRNA expression data and clinical data through TCGA database. Subsequently, we used R language and multiple R language expansion packages to analyze the expression, hazard ratio analysis, and coexpression analysis of PPAR pathway-related genes in KIRC. Afterward, using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) website, we established the protein-protein interaction (PPI) network of genes related to the PPAR pathway. After that, we used LASSO regression curve analysis to establish a prognostic survival model in KIRC. Finally, based on the model, we conducted correlation analysis of the clinicopathological characteristics, univariate analysis, and multivariate analysis.

Results: We found that most of the genes related to the PPAR pathway had different degrees of expression differences in KIRC. Among them, the high expression of 27 genes is related to low survival rate of KIRC patients, and the high expression of 13 other genes is related to their high survival rate. Most importantly, we used 13 of these genes successfully to establish a risk model that could accurately predict patients' prognosis. There is a clear correlation between this model and metastasis, tumor, stage, grade, and fustat.

Conclusions: To the best of our knowledge, this is the first study to analyze the entire PPAR pathway in KIRC in detail and successfully establish a risk model for patient prognosis. We believe that our research can provide valuable data for future researchers and clinicians.

研究目的本研究旨在利用过氧化物酶体增殖激活受体(PPAR)通路相关基因建立肾透明细胞癌(KIRC)的预后风险模型:在这项研究中,我们首先在基因组富集分析(GSEA)网站上找到了 PPAR 通路相关基因,并通过 TCGA 数据库找到了 KIRC mRNA 表达数据和临床数据。随后,我们使用 R 语言和多个 R 语言扩展包分析了 PPAR 通路相关基因在 KIRC 中的表达、危险比分析和共表达分析。随后,我们利用STRING(Search Tool for the Retrieval of Interacting Genes/Proteins)网站,建立了PPAR通路相关基因的蛋白-蛋白相互作用(PPI)网络。之后,我们利用 LASSO 回归曲线分析法建立了 KIRC 的预后生存模型。最后,基于该模型,我们对临床病理特征进行了相关性分析、单变量分析和多变量分析:结果:我们发现大多数与 PPAR 通路相关的基因在 KIRC 中都有不同程度的表达差异。其中,27 个基因的高表达与 KIRC 患者的低存活率有关,另外 13 个基因的高表达与患者的高存活率有关。最重要的是,我们成功地利用其中 13 个基因建立了一个风险模型,该模型可以准确预测患者的预后。该模型与转移、肿瘤、分期、分级和 fustat 有明显的相关性:据我们所知,这是第一项详细分析 KIRC 中整个 PPAR 通路并成功建立患者预后风险模型的研究。我们相信,我们的研究能为未来的研究人员和临床医生提供有价值的数据。
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引用次数: 0
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