Inflammopharmacology最新文献

{"title":"Anti-inflammatory and antioxidant effects of baicalein: targeting Nrf2, and NFĸB in neurodegenerative disease.","authors":"Omkar Kumar Kuwar, Nileshwar Kalia","doi":"10.1007/s10787-025-01698-x","DOIUrl":"https://doi.org/10.1007/s10787-025-01698-x","url":null,"abstract":"<p><p>Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, are characterized by progressive loss of neurons in the brain regions, including the hippocampus, cortex, substantia nigra, and striatum. Multiple pathological mechanisms drive this neuronal loss, including oxidative stress, chronic inflammation, mitochondrial dysfunction, protein misfolding, and excitotoxicity. Recent evidence suggests that these processes are intricately linked to the dysregulation of key signalling pathways, such as the IĸB/NFĸB, and KEAP1/Nrf2 pathways, which play central roles in neuroinflammation, oxidative stress, and mitochondrial functions, respectively. At present, no cure exists for neurodegenerative disorders, and available medications focus solely on symptomatic management. While these treatments provide temporary relief, their long-term use is often associated with adverse health effects. In this context, natural Phytoactive constituents like Baicalein, a bioactive flavonoid derived from Scutellaria baicalensis, have gained attention for their promising therapeutic potential. Baicalein has been shown to modulate the IĸB/NFĸB, and KEAP1/Nrf2 pathways, thereby mitigating neuroinflammation and oxidative stress while supporting mitochondrial health. It exerts anti-inflammatory effects by inhibiting NFĸB activation, thereby reducing the production of proinflammatory cytokines, such as TNF-α, IL-1β, IL-6, and NLRP3 inflammasome, and enzymes like COX-2, LOX, and iNOS, which are essential for innate and adaptive immune responses. Simultaneously, baicalein enhances the Nrf2 activation, promoting the expression of antioxidant enzymes like HO-1, NQO1, GPx, and SOD, thus countering oxidative stress. These findings highlight the potential of baiclalein as a complementary approach for managing neurodegenerative diseases, offering a safer and more holistic alternative to conventional therapies.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissolving microneedle patch for transdermal delivery of perindopril erbumine.","authors":"Zunaira Altaf, Zulcaif Ahmad, Asif Mahmood, Saniia Shchinar, Riffat Latif","doi":"10.1007/s10787-025-01696-z","DOIUrl":"https://doi.org/10.1007/s10787-025-01696-z","url":null,"abstract":"<p><p>Perindopril Erbumine is a widely used angiotensin-converting enzyme (ACE) inhibitor for managing hypertension and cardiovascular diseases. Its dual action of lowering blood pressure and mitigating inflammation makes it a cornerstone treatment in these conditions. However, its oral administration often results in suboptimal bioavailability and gastrointestinal side effects. This study aimed to develop and characterize a dissolving microneedle (dMN) patch for the transdermal delivery of Perindopril Erbumine to enhance therapeutic efficacy and patient compliance. A Perindopril Erbumine-loaded microneedle patch was fabricated using chitosan and polyvinyl alcohol (PVA) using the solvent casting method. The microneedle patch was evaluated for physical properties, mechanical strength, drug loading, and moisture content. Ex-vivo permeation through rat skin and in-vivo pharmacokinetic studies in rabbits was conducted to compare its performance with a marketed oral Perindopril Erbumine formulation. The developed patch demonstrated effective skin penetration, controlled drug release, and a six-fold enhancement in cumulative drug permeation (82.45% ± 1.54) compared to the oral solution (14.32% ± 1.60). The pharmacokinetic study revealed prolonged drug release, with a 7.9-fold increase in half-life (7.739 ± 0.243 h vs. 0.986 ± 0.93 h) and a significantly higher area under the curve (AUC) for the microneedle patch. Skin irritation studies confirmed the biocompatibility of the formulation, with no significant adverse effects observed. These findings highlight the potential of Perindopril Erbumine-loaded dissolving microneedles as a promising transdermal delivery system for improved therapeutic outcomes in managing hypertension and inflammation-related vascular conditions, potentially reducing inflammation through enhanced and targeted drug delivery.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143500832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Certolizumab enhances spinal cord injury recovery in rats through inhibition of the TNF-α signaling pathway and neuronal apoptosis.","authors":"Ozan Küçükatalay, Çağlar Türk, Çevik Gürel, Gökçe Ceren Kuşçu, Mustafa Eren Yüncü, İnanç Karakoyun, Murat Akşit, Onur Sarıkaya, Ali Karadağ, Mahmut Çamlar","doi":"10.1007/s10787-025-01674-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01674-5","url":null,"abstract":"<p><strong>Objective: </strong>Spinal cord injury (SCI), which is characterized by motor and/or sensory dysfunction, presents a significant health challenge resulting from mechanical trauma. Secondary injury, which follows the mechanical trauma and is driven by factors such as inflammation, plays a critical role in the SCI pathophysiology. Scientific evidence indicates that treatment strategies aimed at modulating inflammation during the acute phase of SCI alleviate the seconder injury. In this regard, the present study seeks to evaluate the effectiveness of certolizumab, a monoclonal antibody targeting TNF-α that is widely used in the treatment of various inflammatory diseases, in a SCI model.</p><p><strong>Methods: </strong>In this study, Control, Trauma, and Trauma + Certolizumab groups were established, each comprising eight male rats. One hour after SCI induction, rats in the Trauma + Certolizumab group were administered 10 µg Certolizumab dissolved in saline intraperitoneally, while rats in the Control and Trauma groups received an equivalent volume of saline. After Modified Tarlov Scoring was performed on the seventh day of the experiment, all rats were sacrificed. The effects of certolizumab on neuroinflammation and apoptosis in the SCI model were evaluated using histological, biochemical, and molecular analyses of blood and tissue samples obtained from the rats.</p><p><strong>Results: </strong>Certolizumab downregulated the expression of TNF-α, NF-κB, and IL-6. In addition, as evidenced by the TUNEL assay, Caspase-3 expression (an apoptotic marker), and Modified Tarlov Score results, certolizumab effectively suppressed inflammation-induced neural apoptosis and alleviated locomotor deficits.</p><p><strong>Conclusion: </strong>Certolizumab treatment exerts a neuroprotective effect against secondary damage in SCI through the inhibition of neuroinflammation and apoptosis.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143500829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacillus subtilis (NMCC-path-14) ameliorates acute phase of arthritis via modulating NF-κB and Nrf-2 signaling in mice model.","authors":"Muhammad Usama Mazhar, Sadaf Naz, Tayyaba Zulfiqar, Jehan Zeb Khan, Fahim Hilal, Shakira Ghazanfar, Muhammad Khalid Tipu","doi":"10.1007/s10787-025-01676-3","DOIUrl":"https://doi.org/10.1007/s10787-025-01676-3","url":null,"abstract":"<p><p>Probiotics (PBT) have been extensively studied as an adjunct therapy for various inflammatory conditions. This is because inflammation often leads to dysbiosis, a microbial imbalance that can be corrected using PBT. Most research has focused on Lactobacillus, with limited data on Bacillus PBT for alleviating CFA-induced arthritis in animal models. While most studies focus on the chronic aspect of CFA-induced arthritis, our current research aims to evaluate the effects of pre-treatment, concurrent treatment, and post-treatment with Bacillus subtilis (NMCC-path-14) against the acute phase of arthritis induced by CFA in the mice model. Arthritis was produced by administering CFA into the subplantar region of the mouse's right hind paw. Pain-related behavioral parameters, antioxidant capacity, histological and radiological parameters, expression of essential cytokines, and DNA damage were assessed during the acute phase. B. subtilis treatment significantly reduced the paw edema and improved the arthritic index. The nocifensive threshold was also raised, and muscle coordination improved considerably after B. subtilis treatment on days 7 and 14. The antioxidant capacity and histological and radiological parameters were also enhanced. We demonstrated that B. subtilis therapy preserved the DNA during the acute phase of arthritis using the Comet assay. Comparing results to the arthritic control, a significant reduction was observed in the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and nuclear factor-kappa B (NF-κB). In contrast, the level of nuclear factor erythroid 2-related factor 2 (Nrf-2) was enhanced. During the acute phase of the disease, B. subtilis displayed a potent anti-inflammatory and anti-arthritic action against CFA-induced arthritis.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143500799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of action and new developments in the study of curcumin in the treatment of osteoarthritis: a narrative review.","authors":"Yong-Ze Yang, Ji-Dong Li, Jing-Guo Zhang, Kai Zhang, An-Ren Zhang, Peng-Peng Li, Qing-Jun Li, Hong-Zhang Guo","doi":"10.1007/s10787-025-01665-6","DOIUrl":"https://doi.org/10.1007/s10787-025-01665-6","url":null,"abstract":"<p><p>Osteoarthritis is a degenerative joint disease that affects the aging population worldwide. It has an underlying inflammatory cause that leads to loss of chondrocytes, reducing the cartilage layer at the affected joints. Compounds with anti-inflammatory properties are potential therapeutic agents for osteoarthritis. Curcumin, derived from species of the Curcuma, is an anti-inflammatory compound. The purpose of this review is to summarize the anti-osteoarthritic effects of curcumin from clinical and preclinical studies. Many clinical trials have been conducted to determine curcumin's effectiveness in osteoarthritis patients. Available studies have shown that curcumin prevents chondrocyte apoptosis and inhibits the release of proteoglycans and metalloproteinases as well as the expression of cyclooxygenase, prostaglandin E-2, and inflammatory cytokines in chondrocytes. The mechanism of action of curcumin also involves multiple cell signaling pathways, including Nuclear factor kappa-B(NF-κB), Mitogen-activated protein kinase (MAPK), Wnt/β-catenin pathway (Wnt/β-catenin), The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3), Nuclear factor erythroid 2-related factor 2/antioxidant response elements/heme oxygenase-1(Nrf2/ARE/HO-1), and Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathways. Curcumin further reduced the release of inflammatory factors and apoptosis by inhibiting the activation of NF-κB. In addition, curcumin modulates the MAPK, Nrf2/ARE/HO-1, and PI3K/Akt/mTOR signaling pathways and affects cell proliferation and apoptosis processes, a series of effects that together promote the healthy state of chondrocytes. In conclusion, curcumin, as a natural plant compound, exhibits significant anti-inflammatory potential by modulating inflammatory factors associated with articular osteoarthritis through multiple mechanisms. Its protective effects on articular cartilage and synovium make it a promising candidate for the treatment of OA. Future studies should further explore the mechanism of action of curcumin and its optimal dosage and therapeutic regimen in clinical applications, to provide more effective therapeutic options for osteoarthritis patients.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143500836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis role in complexity of cell death: unrevealing mechanisms in Parkinson's disease and therapeutic approaches.","authors":"Anupam Awasthi, Kousik Maparu, Shamsher Singh","doi":"10.1007/s10787-025-01672-7","DOIUrl":"https://doi.org/10.1007/s10787-025-01672-7","url":null,"abstract":"<p><p>Parkinson's disease (PD), a common neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons, and accumulation of α-synuclein in the substantial nigra. Emerging evidence identifies ferroptosis as a regulated iron-dependent cell death mechanism marked by excessive lipid peroxidation (LPO) as a key contributor to PD pathogenesis. Ferroptosis is intertwined with critical disease processes such as aggregation of α-synuclein protein, oxidative stress generation, mitochondrial alteration, iron homeostasis dysregulation, and neuroinflammation. This mechanism disrupts cellular homeostasis by impairing iron metabolism and antioxidant pathways like the xc^-/glutathione/GPX4 axis and the CoQ10 pathway. This review consolidates current advancements in understanding ferroptosis in these mechanisms, increasing interest in contribution to PD pathology. In addition, it explores the latest developments in ferroptosis-targeting pharmacological agents, including their application in the preclinical and clinical study, and highlights their potential to revolutionize PD management. Unraveling the interplay between ferroptosis and PD offers a transformative perspective, paving the way for innovative therapies to combat this debilitating disease condition.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory effect of multi-dose tranexamic acid in hip and knee arthroplasty: a systematic review and meta-analysis of randomized controlled trials.","authors":"Chen Rui, Guangchun Dai, Chuwei Tian, Shaoyang Zhou, Yucheng Gao, Mumin Cao, Wei Wu, Shengbo Qin, Yunfeng Rui","doi":"10.1007/s10787-025-01679-0","DOIUrl":"https://doi.org/10.1007/s10787-025-01679-0","url":null,"abstract":"<p><strong>Background: </strong>Tranexamic acid (TXA) is considered a potential therapeutic approach to mitigate postoperative inflammatory responses; however, its anti-inflammatory effects remain controversial. This study conducts a systematic review and meta-analysis of randomized controlled trials aiming to investigate the efficacy of multi-dose TXA in exerting anti-inflammatory effects in hip and knee arthroplasty.</p><p><strong>Methods: </strong>We identified potential relevant literature evaluating the anti-inflammatory effects of TXA in patients undergoing hip and knee arthroplasty from PubMed, Embase, and the Cochrane Library. Meta-analysis was performed using RevMan 5.3.</p><p><strong>Results: </strong>Nine randomized controlled studies met the inclusion criteria. Meta-analysis results indicated that, compared with lower doses of TXA, multi-dose TXA significantly reduced the inflammatory markers IL-6 and CRP in patients undergoing hip and knee arthroplasty and shortened the length of hospital stay, with statistically significant results. Nonsignificant differences were found in the incidence of thromboembolic events.</p><p><strong>Conclusion: </strong>Based on the current evidence, our results indicate that multi-dose TXA effectively reduces postoperative inflammatory responses in patients undergoing hip and knee arthroplasty. This anti-inflammatory effect is dose-dependent and is accompanied by a reduction in the length of hospital stay. Nonetheless, further high-quality, multicenter, large-sample-size randomized controlled trials are needed to confirm the anti-inflammatory effects of TXA.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial expression of concern: Chemomodulatory effect Melastoma Malabathricum Linn against chemically induced renal carcinogenesis rats via attenuation of inflammation, oxidative stress, and early markers of tumor expansion.","authors":"Amita Verma, Prakash Chandra Bhatt, Gaurav Kaithwas, Nikunj Sethi, Mohd Rashid, Yashwant Singh, Mahfoozur Rahman, Fahad Al-Abbasi, Firoz Anwar, Vikas Kumar","doi":"10.1007/s10787-025-01684-3","DOIUrl":"https://doi.org/10.1007/s10787-025-01684-3","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Zataria multiflora supplementation on pro- or anti-inflammatory markers: a systematic review and meta-analysis of randomized placebo-controlled trials.","authors":"Alireza Moradi, Farzin Aslani, Mohammad Hossein Boskabady, Yasamin Pahlavan, Mohammad Reza Aslani","doi":"10.1007/s10787-025-01668-3","DOIUrl":"https://doi.org/10.1007/s10787-025-01668-3","url":null,"abstract":"<p><p>The aim of this study was to investigate the effectiveness of Zataria multiflora and carvacrol supplementation on inflammatory markers (IL-2, IL-4, IL-5, IL-6, TNF-α, IL-8, IL-10, interferon gamma (IFN-γ), C-reactive protein (CRP), monocyte chemotactic protein 1 (MCP-1), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF)) by conducting a systematic review and meta-analysis of randomized controlled trials (RCTs).The exploration of literature was conducted until August 2024 on databases like PubMed/Medline, Web of Science, Scopus, Cochrane CENTRAL, and Google Scholar. The current study incorporated trial studies examining how oral supplements of Zataria multiflora and carvacrol impact concentrations of inflammatory markers. By utilizing a random effects model, the mean differences (SMD) and 95% confidence intervals (CI) were pooled for analysis of the results. The Cochrane Q and I² values were used to evaluate heterogeneity. The meta-analysis included ten cases, with 562 participants in the Zataria multiflora group and 700 in the control group. A significant decrease in the levels of various cytokines including IL-2, IL-4, IL-5, IL-6, IL-8, CRP, EGF, VEGF, and MCP-1 was observed with the consumption of Zataria multiflora along with a noteworthy increase in both IFN-γ and IL-10. However, TNF-α levels remained unaffected by the intervention involving Zataria multiflora and carvacrol. It should be noted that limitations of this study include the fact that it draws from research in Iran, encompasses a range of different diseases, and overlooks potential confounders like smoking, physical activity, and diet. In summary, the results suggested that Zataria multiflora and carvacrol can be beneficial for reducing inflammation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating associations between JAK inhibition and venous thromboembolism by systematic mining of large-scale datasets.","authors":"Stine Rabech Haysen, Ane Langkilde-Lauesen Nielsen, Per Qvist, Tue Wenzel Kragstrup","doi":"10.1007/s10787-025-01677-2","DOIUrl":"https://doi.org/10.1007/s10787-025-01677-2","url":null,"abstract":"<p><p>Janus kinase inhibitors (JAKi) have been associated with an increased risk of venous thromboembolism (VTE) limiting the use of JAKi-based therapy. To improve risk stratification and drug development, it is crucial to understand the implication of dysregulated JAK-Signal Transducers and Activators of Transcription (STAT) signaling in the pathogenesis of VTE. The objective of this study is to clarify the putative genomic vulnerability to dysregulated JAK-STAT signaling in VTE through systematic mining of large-scale datasets generated from studies comparing VTE patients with healthy controls. Particularly, we assess the representation of entities of the JAK-STAT signaling pathway including STAT target genes among sets of miRNA, mRNA, and proteins differentially abundant in VTE patients, and we explore the putative cumulative genetic association of JAK-STAT signaling gene sets to VTE. Genes related to the JAK-STAT pathway were found significantly altered in VTE patients compared to healthy controls, indicating that genes under transcriptional control of STAT may be dysregulated in VTE. In support of this notion, we find a significant overrepresentation of predicted STAT target genes among genes downregulated in VTE patients, and promoter sequences of differentially regulated genes were significantly enriched with STAT transcription factor binding site motifs. Further linking STAT signaling to the molecular signature of VTE, genes targeted by miRNAs differentially regulated in patients are significantly enriched with STAT target genes and genes acting in the JAK-STAT signaling pathway. Together, our findings indicate that disruptions in the JAK-STAT pathway contribute to the molecular profile of VTE. This offers hope for identifying ways to interact with the JAK-STAT pathway that do not carry the risk of VTE.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}