Journal of Inflammation Research最新文献

{"title":"Rituximab in the Treatment of Non-Infectious Uveitis: A Review.","authors":"Haixing Cao, Xiang Ma","doi":"10.2147/JIR.S477708","DOIUrl":"10.2147/JIR.S477708","url":null,"abstract":"<p><p>Non-infectious uveitis (NIU) is an immune-mediated disorder manifesting as ocular pain, redness, floaters, and photophobia, and is a leading cause of preventable blindness. Managing NIU presents considerable challenges due to the condition's resistance to high-dose corticosteroids and various immunotherapies. This review assesses the efficacy and safety of rituximab (RTX) in the treatment of NIU, based on individual case reports and small-scale studies. A cohort of 78 patients (20 males, 58 females), with a mean onset age of 32.3 years (range 8-72), was analyzed. Juvenile idiopathic arthritis (JIA) was the most frequently associated comorbidity, affecting 28 patients, while anterior uveitis was the predominant subtype, observed in 26 of 47 cases. Prior to RTX therapy, patients had been treated with an average of 1.7 conventional immunosuppressive agents (range 0-5) and 1.1 biologics (range 0-4). RTX was introduced following the failure of high-dose corticosteroids, immunosuppressive drugs, and biologics to control the uveitis. The median time from diagnosis to RTX initiation was 7.7 years (range 0.25-21). Post-RTX, 44.2% of patients experienced improvement in visual acuity, 79.5% achieved resolution of ocular inflammation, and 8.9% showed partial improvement. Additionally, 81.1% were able to reduce their corticosteroid dosage. Overall, 88.6% (69 out of 78) demonstrated a positive response to RTX treatment. These findings indicate that RTX may serve as an effective therapeutic option for NIU unresponsive to steroids and multiple immunotherapies. It may also warrant consideration as a potential first-line treatment in certain cases.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Pilot HRCT Follow-Up Study to Test the Feasibility of Predictive Efficacy of Serum Periostin in Idiopathic Pulmonary Fibrosis.","authors":"Mingtao Liu, Zhangkai J Cheng, Jiaxi Chen, Haiyang Li, Mingshan Xue, Xing Fu, Yanjun Li, Jiaxin Wang, Chenwei You, Haisheng Hu, Haojie Wu, Huimin Huang, Baoqing Sun","doi":"10.2147/JIR.S458428","DOIUrl":"https://doi.org/10.2147/JIR.S458428","url":null,"abstract":"<p><strong>Background: </strong>While serum periostin and Krebs von den Lungen-6 (KL-6) have been acknowledged as independent markers in idiopathic pulmonary fibrosis (IPF) diagnosis, the clinical combinatory potential of these biomarkers combined with high-resolution computed tomography (HRCT) has yet to be fully explored.</p><p><strong>Methods: </strong>This retrospective study involved 78 participants, comprising 51 UIP-IPF patients and 27 healthy controls. All subjects underwent clinical and laboratory examinations, particularly the detection of periostin and KL-6 using ELISA with innovative HRCT fibrosis score evaluations at admission and discharge during hospitalization in UIP-IPF patients.</p><p><strong>Results: </strong>In our cohort of patients with IPF, predominantly male, over an average follow-up period of 195.27 days. Serum levels of periostin and KL-6 were significantly elevated in IPF patients compared to healthy controls (*p < 0.05). Post-treatment, KL-6 levels decreased significantly, while periostin levels increased. Notably, periostin exhibited superior prognostic accuracy over KL-6, with a higher AUC of 0.875 than 0.639 in ROC analysis. An increase in periostin levels correlated with disease progression, as evidenced by worsened HRCT fibrotic scores and decreased survival probability. These findings underscore periostin's potential as a reliable biomarker for assessing IPF severity and therapeutic response.</p><p><strong>Conclusion: </strong>Our findings underscore the preeminence of serum periostin over KL-6 in UIP-IPF diagnosis, particularly when conjoined with HRCT fibrosis score.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-Cancer Screening and Validation of CALU's Role in EMT Regulation and Tumor Microenvironment in Triple-Negative Breast Cancer.","authors":"Shi-Liang Chen, Dan Hu, Tian-Zhu Chen, Si-Yu Shen, Chen-Fei Zhao, Cong Wang, Shi-Yuan Tong, Zhao Liu, Shao-Hua Lin, Li-Xia Jin, Yi-Bo He, Zhe-Zhong Zhang","doi":"10.2147/JIR.S477846","DOIUrl":"https://doi.org/10.2147/JIR.S477846","url":null,"abstract":"<p><strong>Purpose: </strong>Cancer-associated fibroblasts (CAFs) significantly contribute to tumor progression and the development of resistance to therapies across a range of malignancies, notably breast cancer. This study aims to elucidate the specific role and prognostic relevance of CALU across multiple cancer types.</p><p><strong>Patients and methods: </strong>The association between CALU expression and prognosis, along with clinical characteristics in BRCA, HNSC, KIRP, LGG, and LIHC, was analyzed using data from the TCGA, GTEx, and GEO databases. Transcriptomic analysis of TCGA BRCA project data provided insights into the interaction between CALU and epithelial-mesenchymal transition (EMT) marker genes. Using TIMER and TISCH databases, the correlation between CALU expression and tumor microenvironment infiltration was assessed, alongside an evaluation of CALU expression across various cell types. Furthermore, CALU's influence on TNBC BRCA cell lines was explored, and its expression in tumor tissues was confirmed through immunohistochemical analysis of clinical samples.</p><p><strong>Results: </strong>This study revealed a consistent upregulation of CALU across several tumor types, including BRCA, KIRP, LIHC, HNSC, and LGG, with elevated CALU expression being associated with unfavorable prognoses. CALU expression was particularly enhanced in clinical contexts linked to poor outcomes. Genomic analysis identified copy number alterations as the principal factor driving CALU overexpression. Additionally, a positive correlation between CALU expression and CAF infiltration was observed, along with its involvement in the EMT process in both CAFs and malignant cells. In vitro experiments demonstrated that CALU is highly expressed in TNBC-BRCA cell lines, and knockdown of CALU effectively reversed EMT progression and inhibited cellular migration. Immunohistochemical analysis of clinical samples corroborated the elevated expression of CALU in tumors, along with alterations in EMT markers.</p><p><strong>Conclusion: </strong>This comprehensive pan-cancer analysis underscores CALU's critical role in modulating the tumor microenvironment and facilitating cell migration via the EMT pathway, identifying it as a potential therapeutic target.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Qing-Luo-Yin Eased Adjuvant-Induced Arthritis by Inhibiting SIRT1-Controlled Visfatin Production in White Adipose Tissues.","authors":"Dan-Dan Wang, Meng-Ke Song, Qin Yin, Wen-Gang Chen, Opeyemi Joshua Olatunji, Kui Yang, Jian Zuo","doi":"10.2147/JIR.S474329","DOIUrl":"https://doi.org/10.2147/JIR.S474329","url":null,"abstract":"<p><strong>Background: </strong>Nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 regulates both metabolism and immune functions. This study investigated if SIRT1 inhibitory property of herbal formula Qing-Luo-Yin (QLY) contributed to its anti-rheumatic effects.</p><p><strong>Methods: </strong>Adjuvant-induced arthritis (AIA) rats were treated by QLY and nicotinamide mononucleotide (NMN, a biosynthesis precursor of NAD) for 38 days. After sacrifice, blood, paws, liver and white adipose tissues (WAT) were collected. Pre-adipocytes were cultured by the rats' serum. The medium was used for monocytes culture. Some pre-adipocytes were treated by QLY-derived SIRT1 inhibitors. <i>SIRT1</i> was silenced or overexpressed beforehand. The samples were subjected to kits-based quantification, polymerase-chain reaction, western-blot, immunofluorescence, and histology experiments.</p><p><strong>Results: </strong>AIA rats experienced significant fat loss in liver and WAT. Expression of many SIRT1-related signals like PPARγ, PGC-1α, HSL, ATGL and CPT-1A were altered. QLY attenuated all these abnormalities and joint injuries. By pan-acetylation up-regulation, visfatin was obviously reduced in QLY-treated AIA rats' blood (from 191.8 to 127.0 pg/mL). NMN sustained SIRT1 activation by replenishing NAD, and weakened these effects. QLY-containing serum and the related compounds showed similar impacts on pre-adipocytes, resembling the changes in QLY-treated AIA rats' WAT. These treatments suppressed AIA serum-induced visfatin secretion (from 49.3 to 36.1 and 30.7 pg/mL). This effect was impaired by <i>SIRT1</i> overexpression. The medium from the compounds-treated pre-adipocytes impaired NF-κB activation in AIA serum-cultured monocytes.</p><p><strong>Conclusion: </strong>Besides fat depletion, SIRT1 up-regulation in rheumatic subjects' WAT promotes visfatin production, and exacerbates inflammation. SIRT1 inhibition in WAT is an anti-rheumatic way of QLY independent of immune regulation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Efficacy and Safety of Ustekinumab and Secukinumab in the Treatment of Generalized Pustular Psoriasis: A 48-Week Retrospective Cohort Study with Genetic Background Analysis.","authors":"Shi-Fan Ruan, Xinhong Su, Zhixun Xiao, Yihua Zhang, Tingting Lin, Renwei Luo, Niu Xiang, Bo Cheng, Ting Gong, Chao Ji","doi":"10.2147/JIR.S472338","DOIUrl":"https://doi.org/10.2147/JIR.S472338","url":null,"abstract":"<p><strong>Purpose: </strong>Recent studies have shown that novel biologics may provide significant clinical benefits for patients with generalized pustular psoriasis (GPP). Ustekinumab and secukinumab have been approved in Japan for GPP treatment in adult patients. However, the differences in efficacy and safety of these two drugs in GPP are not known.</p><p><strong>Aim: </strong>Based on the genetic background, we aimed to compare the efficacy and safety of secukinumab and ustekinumab in patients with GPP.</p><p><strong>Methods: </strong>Patients with moderate to severe GPP who were treated with ustekinumab/secukinumab at our department from July 2019 to May 2022 were included in this study and followed up for 48 weeks. The difference in efficacy between ustekinumab and secukinumab was evaluated by assessing changes in body temperature, laboratory indices, recovery of skin lesions, and changes in quality of life. Additionally, we collected patients' saliva for genotyping and explored the effect of CARD14 genetic mutations on clinical efficacy.</p><p><strong>Results: </strong>A total of 65 patients (32 adults and 33 children) with moderate to severe GPP were included in this study. 31 patients received ustekinumab therapy, and 34 patients were treated with secukinumab. Secukinumab demonstrated superiority to ustekinumab, as evidenced by a higher GPPASI 90 response at week 2. Additionally, the efficacy of ustekinumab and secukinumab was found to be independent of the presence of the CARD14 mutation.</p><p><strong>Conclusion: </strong>Secukinumab is superior to ustekinumab in rapidly clearing the skin and improving health-related quality of life. Moreover, the responses to ustekinumab/secukinumab in patients were not influenced by CARD14 gene mutations.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unexpected Foreign Body-Induced Small Bowel adenocarcinoma: A Case Report.","authors":"Yu Zhang, Hong-Hai Li, Min-Feng Ye, Wei-Wei Li, Chu Zhang, Hai-Feng Wang","doi":"10.2147/JIR.S477855","DOIUrl":"https://doi.org/10.2147/JIR.S477855","url":null,"abstract":"<p><strong>Background: </strong>Foreign body-induced cancer is a traditional way of understanding cancer development. The induction of cancers by exogenous foreign bodies has been identified in many organs. However, small bowel adenocarcinoma induced by foreign bodies has not been reported in the literature, although the incidence of small bowel adenocarcinoma is increasing globally.</p><p><strong>Case presentation: </strong>A 70-year-old man was hospitalized for persistent right-sided abdominal pain for 3 months. Abdominal computed tomography revealed localized thickening and clustering of the small bowel wall in the right abdominal cavity. A comminuted fracture of the right 11th rib protruding into the abdominal cavity was observed, with a bone fragment located within the intestinal mass. Exploratory laparotomy was performed, and extensive adhesions were noted among the greater omentum, small bowel, mesentery, and right abdominal wall. Radical resection and lymph node dissection of the affected small bowel and appendix were performed. We also excised the rib end and repaired the abdominal wall to prevent further irritation. The patient was discharged 12 days post-surgery and follow-up assessments revealed no reported discomfort.</p><p><strong>Conclusion: </strong>We first report a case of small bowel adenocarcinoma induced by self-bone tissue, along with successful radical tumor excision and thorough foreign body removal. This case highlights the significant role of chronic inflammation in carcinogenesis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Outcomes of Diabetes Mellitus on Moderately Severe Acute Pancreatitis and Severe Acute Pancreatitis.","authors":"Jiale Xu, Musen Xu, Xin Gao, Jiahang Liu, Jingchao Sun, Ruiqi Ling, Xuchen Zhao, Xifeng Fu, Shaojian Mo, Yanzhang Tian","doi":"10.2147/JIR.S478983","DOIUrl":"https://doi.org/10.2147/JIR.S478983","url":null,"abstract":"<p><strong>Objective: </strong>To analyze the influence of diabetes mellitus on the clinical outcomes of moderately severe acute pancreatitis (MSAP) and severe acute pancreatitis (SAP).</p><p><strong>Methods: </strong>This retrospective study included patients diagnosed with MSAP and SAP at Shanxi Bethune Hospital from January 1, 2017, to December 31, 2021. Clinical data were collected, including patient demographics, 24-hour laboratory indicators, and inflammation indices. Propensity score matching (PSM) was used to compare outcomes before and after matching. Patients were randomized into training and validation sets (7:3) to develop and validate a clinical prediction model for infected pancreatic necrosis (IPN).</p><p><strong>Results: </strong>Among 421 patients, 79 had diabetes at admission. Before PSM, diabetic patients had higher incidences of peripancreatic fluid (71% vs 47%, p<0.001) and IPN (48% vs 10%, p<0.001), higher surgical intervention rates (24% vs 12%, p=0.008), and significant differences in abdominocentesis (22% vs 11%, p=0.014). After PSM, 174 patients were matched, and the diabetes group still showed higher incidences of peripancreatic fluid (69% vs 47%, p=0.008), IPN (48% vs 11%, p<0.001), and surgical intervention rates (27% vs 13%, p=0.037). Diabetes, modified CT severity index (MCTSI), serum calcium, and HDL-c were identified as independent risk factors for IPN. The prediction model demonstrated good predictive value.</p><p><strong>Conclusion: </strong>In MSAP and SAP patients, diabetes mellitus can exert an influence on their clinical outcome and is an independent risk factor for IPN. The alignment diagram and web calculator constructed on the basis of diabetes mellitus, modified CT severity index (MCTSI), serum calcium and high-density lipoprotein cholesterol (HDL-c) have good predictive value and clinical guidance for the occurrence of IPN in MSAP and SAP.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11430846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil-to-Lymphocyte Ratio, Lymphocyte-to-Monocyte Ratio and Platelet-to-Lymphocyte Ratio as Predictors of Short- and Long-Term Outcomes in Ischemic Stroke Patients with Atrial Fibrillation.","authors":"Jiahuan Guo, Dandan Wang, Jiaokun Jia, Jia Zhang, Yanfang Liu, Jingjing Lu, Xingquan Zhao, Jing Yan","doi":"10.2147/JIR.S480513","DOIUrl":"https://doi.org/10.2147/JIR.S480513","url":null,"abstract":"<p><strong>Purpose: </strong>Inflammatory response plays essential roles in the pathophysiology of both ischemic stroke and atrial fibrillation (AF). We aimed to investigate whether composite inflammatory markers, including neutrophil to lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR) and platelet-to-lymphocyte ratio (PLR), can serve as early predictors of short- and long-term outcomes in ischemic stroke patients with AF.</p><p><strong>Patients and methods: </strong>Ischemic stroke patients with AF were enrolled in this cohort study. The primary outcome was 1-year functional dependence or death (modified Rankin scale (mRS) score 3-6). Secondary outcomes included hemorrhagic transformation (HT) and early neurological deterioration (END, increase in the National Institutes of Health Stroke Scale (NIHSS) ≥4 within 7 days). Partial correlations were performed to assess the correlation between systemic inflammation markers and admission NIHSS scores. Univariate and multivariate logistic analyses were performed to investigate whether systemic inflammatory markers were independent predictors of adverse outcomes.</p><p><strong>Results: </strong>A total of 408 patients were included. Partial correlation analysis revealed statistically significant but weak correlations between the NLR (r = 0.287; P < 0.001), PLR (r = 0.158; P = 0.001) and admission NIHSS score. Compared with patients without HT or END, patients who developed HT or END had higher NLR and PLR, and lower LMR. Patients in the functional dependence or death group had significantly higher NLR and PLR, and lower LMR than those in the functional independence group (all P < 0.001). Multivariate logistic analysis indicated that NLR, LMR and PLR were independent predictors of HT (OR = 1.069, 0.814 and 1.003, respectively), END (OR = 1.100, 0.768 and 1.006, respectively) and adverse 1-year functional outcome (OR = 1.139, 0.760 and 1.005, respectively).</p><p><strong>Conclusion: </strong>NLR, LMR and PLR were independent predictors for in-hospital HT, END and long-term functional outcome in ischemic stroke patients with AF. Close monitoring of these inflammatory markers may help guide risk stratification and clinical treatment strategies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11430226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic Analysis of Cardiac Tissues in a Rodent Model of Coronary Microembolization.","authors":"Zhaochang Jiang, Haohao Lu, Beibei Gao, Jinyu Huang, Yu Ding","doi":"10.2147/JIR.S469297","DOIUrl":"https://doi.org/10.2147/JIR.S469297","url":null,"abstract":"<p><strong>Purpose: </strong>Coronary microembolization (CME) can result in cardiac dysfunction, severe arrhythmias, and a reduced coronary flow reserve. Impairment of mitochondrial energy metabolism has been implicated in the progression and pathogenesis of CME; however, its role remains largely undetermined. This study aimed to explore alterations in mitochondria-related genes in CME.</p><p><strong>Methods: </strong>A rat model of CME was successfully established by injecting plastic microspheres into the left ventricle. The cardiac tissues of the two groups were sequenced and mitochondrial functions were assessed.</p><p><strong>Results: </strong>Using RNA-Seq, together with GO and KEGG enrichment analyses, we identified 3822 differentially expressed genes (DEGs) in CME rats compared to control rats, and 101 DEGs were mitochondria-related genes. Notably, 36 DEGs were up-regulated and 65 DEGs were down-regulated (CME vs control). In particular, the oxidative phosphorylation (OXPHOS) and mitochondrial electron transport were obviously down-regulated in the CME group. Functional analysis revealed that CME mice exhibited marked reductions in ATP and mitochondrial membrane potential (MMP), by contrast, the production of reactive oxygen species (ROS) was much higher in CME mice than in controls. Protein-protein interaction (PPI) and quantitative PCR (qPCR) validation suggested that eight hub genes including Cmpk2, Isg15, Acsl1, Etfb, Ndufa8, Adhfe1, Gabarapl1 and Acot13 were down-regulated in CME, whereas Aldh18a1 and Hspa5 were up-regulated.</p><p><strong>Conclusion: </strong>Our findings suggest that dysfunctions in mitochondrial activity and metabolism are important mechanisms for CME, and mitochondria-related DEGs may be potential therapeutic targets for CME.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11437660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multifaceted Protective Role of Nuclear Factor Erythroid 2-Related Factor 2 in Osteoarthritis: Regulation of Oxidative Stress and Inflammation.","authors":"Weibei Sheng, Yaohang Yue, Tiantian Qi, Haotian Qin, Peng Liu, Deli Wang, Hui Zeng, Fei Yu","doi":"10.2147/JIR.S479186","DOIUrl":"https://doi.org/10.2147/JIR.S479186","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a chronic degenerative joint disease characterized by the degradation of joint cartilage, subchondral bone sclerosis, synovitis, and structural changes in the joint. Recent research has highlighted the role of various genes in the pathogenesis and progression of OA, with nuclear factor erythroid 2-related factor 2 (NRF2) emerging as a critical player. NRF2, a vital transcription factor, plays a key role in regulating the OA microenvironment and slowing the disease's progression. It modulates the expression of several antioxidant enzymes, such as Heme oxygenase-1 (HO-1) and NAD(P)H oxidoreductase 1 (NQO1), among others, which help reduce oxidative stress. Furthermore, NRF2 inhibits the nuclear factor kappa-B (NF-κB) signaling pathway, thereby decreasing inflammation, joint pain, and the breakdown of cartilage extracellular matrix, while also mitigating cell aging and death. This review discusses NRF2's impact on oxidative stress, inflammation, cell aging, and various cell death modes (such as apoptosis, necroptosis, and ferroptosis) in OA-affected chondrocytes. The role of NRF2 in OA macrophages, and synovial fibroblasts was also discussed. It also covers NRF2's role in preserving the cartilage extracellular matrix and alleviating joint pain. The purpose of this review is to provide a comprehensive understanding of NRF2's protective mechanisms in OA, highlighting its potential as a therapeutic target and underscoring its significance in the development of novel treatment strategies for OA.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}