MEDIATORS OF INFLAMMATION炎症介质
MEDIATORS OF INFLAMMATION(英文缩写 MEDIAT INFLAMM),ISSN 0962-9351,eISSN 1466-1861,中文译名:炎症介质 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.529 | Q3 |
| 2022 | 4.600 | Q2 |
| 2023 | 4.400 | Q2 |
| 2024 | 4.200 | Q2 |
| 2025 | 4.900 | Q2 |
MEDIATORS OF INFLAMMATION 最新收录文献
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1. Population-Level Burden of Dermatitis and the Effects of Moxibustion and Capsaicin on Pruritus and JAK/STAT Signaling in Atopic Dermatitis: A Multilevel Study.
PMID:日期:2026-01-01This study comprised two complementary levels of investigation. First, we characterized the global burden, temporal trends, and socioeconomic inequalities of dermatitis as an aggregated disease category. Second, within this broader public-health context, we investigated whether moxibustion and topical capsaicin alleviate pruritus and inflammatory skin damage in a rat model of atopic dermatitis (AD) and explored their potential convergent regulation of the Janus kinase (JAK)/STAT signaling pathway. The study comprised a population-level contextual analysis and a disease-specific experimental investigation. Age-standardized incidence rates (ASIRs) and disability-adjusted life years (DALYs) attributable to each risk factor for dermatitis were extracted and assessed from the Global Burden of Disease (GBD) database. The GBD component was used to characterize the broader public-health burden of dermatitis and was not interpreted as an AD-specific epidemiological analysis. An AD rat model was established using 2,4-dinitrochlorobenzene (DNCB) in an acetone solution. Successfully modeled rats were randomly assigned to untreated model, mometasone furoate cream, moxibustion, or topical capsaicin groups. The standard pharmacological treatment group was included as a therapeutic efficacy benchmark, whereas capsaicin was used as a sensory-neuron-modulating active comparator for the exploratory analysis of downstream molecular convergence. Proteomic analysis was used to identify treatment-associated pathways, and changes in IFN-γ/JAK1/STAT1/STAT3 signaling components were subsequently assessed by western blotting, RT-qPCR, and immunohistochemistry. In addition to skin-lesion severity and scratching behavior, pruritus-related neuroimmune mediators were evaluated. Serum IL-31 concentrations were measured by ELISA. Cutaneous IL-31 and TRPV1 expression was assessed by immunohistochemistry, and substance P immunoreactivity was evaluated by immunofluorescence. The relative mRNA expression of Trpv1, SP(Tac1), and CGRP in lesional skin was measured by RT-qPCR. The global incidence of dermatitis increased, with a higher burden in females. Significant inequalities in incidence and DALYs existed across countries of varying sociodemographic index (SDI) levels. At the experimental level, target intersection analysis identified 302 genes shared by capsaicin, AD, and pruritus, while lesional-skin proteomics identified 257 common differentially expressed proteins. Exploratory proteomic enrichment identified JAK/STAT signaling as the most prominent candidate pathway in the enrichment bubble plot. AD model rats exhibited increased scratching, upregulated pruritus-related mediators (IL-31, TRPV1, substance P, and Trpv1/Tac1/CGRP transcripts), exacerbated skin lesions, histopathological damage, and a pro-inflammatory shift (elevated IL-1, IL-4, IL-6, TNF-α, IFN-γ; reduced IL-10). Mometasone furoate predictably alleviated these AD-like manifestations. Both moxibustion and capsaicin treatments reversed these trends, improving pathology, restoring spleen/thymus indices, and downregulating IFN-γ expression and JAK1/STAT1/STAT3 phosphorylation. Aggregated dermatitis continues to impose a substantial and unevenly distributed global health burden. Within this broader public-health context, the experimental findings indicate that moxibustion and topical capsaicin alleviate pruritus and inflammatory skin damage in rats with AD. These improvements were accompanied by attenuation of IFN-γ/JAK1/STAT1/STAT3-associated signaling, supporting the potential involvement of the JAK/STAT pathway in the observed treatment responses.
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2. Tempol Ameliorates Psoriatic Skin Inflammation: Evidence of TLR4/NF-κB/Nrf2 Axis Modulation.
PMID:日期:2026-01-01Psoriasis is a chronic inflammatory skin disorder characterized by keratinocyte hyperproliferation, immune dysregulation, oxidative stress, and impaired epidermal barrier function. In the present study, we investigated the protective effects of Tempol, a membrane-permeable nitroxide with antioxidant and anti-inflammatory properties, using several psoriasiform models. In HaCaT keratinocytes, stimulation with a cytokine mixture significantly induced inflammatory responses. Tempol (0.5 and 1 mM) showed no cytotoxic effects and markedly reduced the mRNA and protein levels of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6. Tempol was associated with reduced expression of TLR4, MyD88, TRAF6, and nuclear factor-kappa B (NF-κB), together with restoration of IκBα expression, findings consistent with modulation of the TLR4/NF-κB signaling pathway. In parallel, Tempol was associated with activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/HO-1 antioxidant axis, as evidenced by increased expression of Nrf2, HO-1, and MnSOD, along with a reduction in the pro-oxidant enzymes NOX2 and NOX4. These effects were associated with decreased oxidative damage, including reduced lipid peroxidation and nitric oxide production. Furthermore, Tempol exerted cytoprotective effects by restoring the balance between pro- and antiapoptotic markers, as indicated by increased Bcl-2 levels, decreased Bax and p53 expression, and a reduced Bax/Bcl-2 ratio. The anti-inflammatory activity of Tempol was further confirmed in an imiquimod (IMQ)-stimulated HaCaT/THP-1 coculture model, where it significantly reduced the release of key immune mediators, including TLR4, IL-8, IL-17A, and IL-23, highlighting its ability to modulate immune-epithelial crosstalk. In a reconstructed human epidermis (RHE) model, Tempol preserved tissue viability under psoriasiform conditions and significantly reduced Staphylococcus aureus (S. aureus) adhesion. Importantly, Tempol restored epidermal barrier integrity, as demonstrated by increased levels of tight junction and differentiation markers, including ZO-1, Occludin, Claudin-1, and Filaggrin, even under infection-associated conditions. Taken as a whole, these findings support the potential of Tempol as a promising therapeutic strategy for psoriasis and related inflammatory skin disorders.
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3. TREM2: A Potential Target for the Targeted Therapy of Metabolic Diseases.
3. TREM2：代谢性疾病靶向治疗的潜在靶点PMID:日期:2026-01-01Metabolic diseases are characterized by profound dysregulation of the immunometabolic network, in which the interplay between chronic inflammation and metabolic disturbances form a self-amplifying vicious cycle that drives disease progression. disease progression. Triggering receptor expressed on myeloid cells 2 (TREM2), a central regulator of immunometabolism, interacts with the adaptor protein DAP12 to orchestrate key macrophage functions including polarization, phagocytic clearance, inflammation resolution, and metabolic reprogramming. Through these processes, TREM2 plays a critical role in sensing metabolic stress signals and maintaining immunometabolic homeostasis. In this review, we systematically summarize recent advances in understanding the roles of TREM2 in major metabolic diseases, including atherosclerosis (AS), diabetes mellitus and its complications, obesity, and non-alcoholic steatohepatitis (NASH), while highlighting its functional heterogeneity across different diseases contexts. We further dissect the regulatory mechanisms governing TREM2 activity, with particular emphasis on cell subset-specific expression patterns, microenvironmental signal interactions, and post-translational modifications (PTMs). Moreover, we summarize emerging TREM2-targeted therapeutic strategies, including soluble TREM2 (sTREM2), agonistic antibodies, and traditional Chinese medicine (TCM)-based approaches, and evaluate the translational potential of sTREM2 as a noninvasive biomarker. Emerging research frontiers involving TREM2, such as the gut microbiota-metabolism axis and interorgan communication, are also discussed. Finally, we identify key unresolved questions and future research priorities, providing a theoretical framework and potential strategies for precision diagnosis and targeted intervention in metabolic diseases.
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4. Role of Prokineticin-2 and Cytokines in Synovial Fluid in Traumatic Anterior Cruciate Ligament Injuries.
PMID:日期:2026-01-01Anterior cruciate ligament (ACL) tears induce a proinflammatory intra-articular environment. Despite successful ACL reconstruction (ACLR), post-traumatic osteoarthritis (PTOA) incidence remains high. The role of prokineticin-2 (PK2), a novel inflammatory and pain mediator, was investigated in this observational study of traumatic ACL injuries, associated with meniscal tears. Twenty patients with isolated ACL tears (ACL group) and 20 with associated meniscal injury (ACL + M group) were enrolled. Synovial fluid PK2, IL-10, and TNF-α levels were measured using ELISA method. Patients underwent long-term follow-up (minimum 5 years) with clinical reassessment using patient-reported outcome measures (PROMs) (IKDC, Lysholm, Tegner activity scale, SKV). PK2 was detected in both ACL and ACL + M groups without significant differences. Higher PK2 levels were associated with hemarthrosis and correlated positively with IL-10. No associations were found between PK2 levels and demographic factors or time from injury. At follow-up, PK2 negatively correlated with IKDC, Lysholm, and SKV scores. This study provides initial evidence of PK2 in synovial fluid following ACL injury, suggesting its potential role in knee inflammation. PK2 may represent a candidate biomarker involved in the post-traumatic inflammatory microenvironment; however, further longitudinal studies including structural outcomes are needed.
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5. Demethoxycurcumin Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Nrf2-Mediated Anti-Inflammation and Ferroptosis Inhibition.
PMID:日期:2026-01-01Sepsis-induced acute lung injury (SI-ALI) represents a life-threatening condition driven by dysregulated immune responses and redox imbalance. Demethoxycurcumin (DMC), a bioactive analog of curcumin, exhibits marked anti-inflammatory and free radical-scavenging capacities. Despite its potential, the precise molecular pathways through which DMC mitigates SI-ALI pathogenesis have yet to be fully elucidated. SI-ALI was induced in mice through lipopolysaccharide (LPS) administration. Lung injury was assessed by histopathological analysis and measurement of wet-to-dry (W/D) weight ratios. Oxidative stress markers were quantified using ELISA, and inflammatory cytokine mRNA levels were analyzed by RT-PCR. Ferroptosis-related proteins and Nrf2 pathway activation were evaluated through Western blotting and immunofluorescence. Mitochondrial ultrastructure was examined via transmission electron microscopy (TEM). The involvement of the Nrf2 pathway was further confirmed by using the Nrf2 inhibitor ML385. DMC treatment significantly alleviated lung injury in a dose-dependent manner, improving histopathology and reducing W/D weight ratios. It attenuated inflammation by suppressing IL-6, TNF-α, and IL-1β expression and restored oxidative balance by enhancing glutathione (GSH) levels while decreasing malondialdehyde (MDA). Moreover, DMC upregulated glutathione peroxidase 4 (GPX4) and SLC7A11, downregulated cyclooxygenase-2 (COX2) and ACSL4, reduced nonheme iron and 4-hydroxynonenal (4-HNE) production, and improved mitochondrial morphology, collectively demonstrating its inhibitory effects on ferroptosis. Nrf2 inhibition partially reversed these protective effects, underscoring the central role of the Nrf2 pathway in DMC's mechanism of action. DMC ameliorates SI-ALI by mitigating inflammation and ferroptosis through Nrf2 pathway activation, suggesting a potential therapeutic strategy for SI-ALI treatment.
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6. Exploring Causal Links Between 91 Circulating Inflammatory Proteins and Hashimoto's Thyroiditis: A Bidirectional Mendelian Randomization Study.
PMID:日期:2026-01-01Increasing evidence has linked inflammation to Hashimoto's thyroiditis (HT) etiology. However, the causal role of circulating inflammatory proteins in HT remains uncertain. To investigate this, we conducted a bidirectional Mendelian randomization (MR) study. Genetic data for 91 inflammatory proteins and HT were sourced from publicly available GWAS databases. The PhenoScanner database was then searched for pleiotropic SNPs associated with potential confounders. Inverse variance weighted (IVW) analysis was used as the primary analysis, simultaneously supplemented by five sensitivity analyses to strengthen the results. The results revealed that, after false discovery rate (FDR) correction, interleukin (IL)-12p40 was causally associated with increased risk of HT (OR [95% CI] = 1.295 [1.172, 1.431], p = 3.66 × 10, P = 3.33×10). Conversely, none of the inflammatory proteins was a consequence of HT. This study suggests that IL-12p40 is probably one of the factors correlated with HT etiology, contributing to a better understanding of the pathogenesis of HT and underscoring the potential for therapeutic interventions targeting inflammatory proteins.
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7. Identification of Integrated Stress Response-Related Biomarkers in Sepsis-Induced Acute Respiratory Distress Syndrome.
7. 脓毒症诱导的急性呼吸窘迫综合征中综合应激反应相关生物标志物的鉴定PMID:日期:2026-01-01Sepsis-induced acute respiratory distress syndrome (ARDS) is a fatal inflammatory lung injury. The integrated stress response (ISR) may play stage-dependent roles in lung injury, but its clinical relevance in sepsis-induced ARDS remains unclear. We aimed to identify ISR-related biomarkers and explore their potential mechanisms. Public transcriptomic datasets of sepsis-induced ARDS were analyzed. Peripheral blood mononuclear cell (PBMC) single-cell RNA sequencing (scRNA-seq) was used to define key immune cell populations and intercellular communication. Differential expression analyses combined with machine learning were applied to screen ISR-associated biomarkers, and a nomogram was developed as an exploratory tool for ARDS risk stratification. Biomarker expression was validated in a cecal ligation and puncture (CLP)-based rat model representing early sepsis and ARDS-like lung injury. Lung injury was assessed by light and electron microscopy, histological scoring, lung wet/dry weight ratio, and BALF total protein measurement. Gene expression was quantified by qPCR and protein levels by Western blotting. Functional enrichment, immune infiltration, and trajectory analyses were performed to investigate underlying pathways and immune dynamics. The biomarkers were further validated in an independent external dataset. Nuclear factor erythroid 2-like 2 (NFE2L2) and ZFP36L1 were identified as potential ISR-associated biomarkers in sepsis-induced ARDS, and the two-gene nomogram showed good predictive performance. In vivo, peripheral blood Tnf and Il6 mRNA expression increased after CLP, while rats with ARDS-like lung injury exhibited marked lung injury and reduced tight junction markers. Nfe2l2 and Zfp36l1 mRNA levels were elevated in early sepsis but decreased in established ARDS-like lung injury, while their protein levels were generally reduced in established ARDS-like lung injury compared with early sepsis. Canonical ISR activation markers, including the p-eukaryotic translation initiation factor 2α (eIF2α)/total eIF2α ratio and Atf4, Ddit3/Chop, and Ppp1r15 a/Gadd34 expression, progressively increased from early sepsis to ARDS-like lung injury. Enrichment analyses implicated multiple ISR-related pathways. Immune infiltration analysis revealed altered immune cell composition, with NFE2L2 negatively correlated with activated B cell infiltration. Single-cell trajectory analysis demonstrated dynamic expression of these biomarkers during differentiation of key immune cell subsets. NFE2L2 and ZFP36L1 are potential ISR-associated biomarkers in sepsis-induced ARDS and may contribute to disease progression through stress-response regulation and immune modulation, supporting biomarker-driven risk stratification and providing a foundation for future mechanistic and interventional studies.
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8. Associations Between Metabolic Syndrome Index, Systemic Inflammatory Index, and Arthritis Subtype in the U.S. and Chinese Adults: A Mediation Analysis.
PMID:日期:2026-01-01Arthritis represents a spectrum of chronic inflammatory conditions, with growing evidence linking metabolic dysregulation to disease pathogenesis. While composite metabolic indices have been proposed as potential markers for arthritis, their associations with specific disease subtypes and applicability across diverse ethnic populations remain insufficiently characterized. This study analyzed data from 15,015 participants in the U.S. National Health and Nutrition Examination Survey (NHANES) and 3848 subjects from a Chinese hospital-based cohort. Associations between triglyceride-glucose (TyG) index/TyG-body mass index (TyG-BMI) and arthritis subtypes (osteoarthritis [OA], rheumatoid arthritis [RA], and gout) were assessed using multiple logistic regression and restricted cubic splines (RCS) with adjustment for age and gender. Mediation analysis evaluated the role of the systemic immune-inflammation index (SII). Predictive performance was compared using area under the curve (AUC). Elevated TyG and TyG-BMI were significantly associated with higher odds of multiple arthritis subtypes in both cohorts. In NHANES, the highest TyG quartile was linked to 26%-64% higher odds compared with the lowest quartile, while TyG-BMI showed stronger associations (ORs 2.25-2.76). Similarly, TyG-BMI was strongly associated with RA (OR = 4.77) and gout (OR = 5.46) in the Chinese cohort. Dose-response analyses confirmed significant nonlinear positive relationships between TyG/TyG-BMI levels and arthritis risk. Systemic inflammation mediated a substantial proportion of these associations (all p < 0.05). Predictive performance differed ethnically: TyG-BMI performed best in the U.S. cohort (AUCs 0.599-0.617), whereas the TyG index was superior in the Chinese cohort (AUCs 0.647-0.719). This cross-population study demonstrates that TyG and TyG-BMI indices are positively and dose-dependently associated with multiple arthritis subtypes, with systemic inflammation serving as a partial mediator. These findings underscore the utility of TyG and TyG-BMI indices in identifying at-risk individuals for targeted early intervention and personalized management of arthritis.
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9. Integrated Transcriptomic Analyses and Experimental Validation Identify TSPO as a Mitochondria-Associated Therapeutic Target in Myocarditis.
9. 整合转录组学分析和实验验证确定TSPO为心肌炎中线粒体相关治疗靶点PMID:日期:2026-01-01Myocarditis is characterized by inflammatory cell infiltration and myocardial injury, yet current treatments remain largely empirical and nonspecific. Given the heart's high energy demand and the essential role of mitochondria in cellular metabolism, investigating mitochondria-related genes may provide novel therapeutic insights. In this study, we integrated bulk RNA sequencing data from CVB3 viral myocarditis (VMC) model with mitochondrial gene sets from MitoCarta3.0 and human myocarditis-related genes from GeneCards. Through comprehensive bioinformatics analyses, including weighted gene coexpression network analysis (WGCNA), random forest (RF), and SHapley Additive exPlanations (SHAP), we identified mitochondrial metabolism-related genes associated with myocarditis. Single-cell RNA sequencing (scRNA-seq) analysis further revealed that macrophages were the predominant infiltrating immune population, with Tspo expressed in myocarditis macrophages. Tspo knockdown enhanced inflammatory responses and disrupted mitochondrial structure and function, whereas treatment with the Tspo ligand Ro5-4864 exerted the opposite effects. Consistently, administration of Ro5-4864 in a VMC mouse model mitigated inflammation and preserved cardiac function. Collectively, our findings identify Tspo as a novel mitochondria-associated protective response factor in myocarditis, providing new insights into its pathophysiological mechanisms and highlighting Tspo as a promising therapeutic target for future intervention.
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10. Protein Fragments: From Biomarkers to Therapeutic Targets-A Focus on α1-Antitrypsin-Derived Peptides.
PMID:日期:2026-01-01Protein fragments are increasingly recognized as both biomarkers and therapeutic targets, offering important insights into disease mechanisms and potential intervention strategies. Evidence from in vitro and in vivo studies indicates that these fragments are not merely degradation products but possess distinct biological activities, actively modulating immune signaling and contributing to both acute and chronic inflammatory processes. Here, we provide an overview of proteases and their inhibitors, with a particular focus on peptide fragments generated through proteolytic cleavage. Special emphasis is placed on fragments derived from α1-antitrypsin (AAT), an acute-phase glycoprotein and major inhibitor of neutrophil elastase and other serine proteases. AAT-derived peptides of varying lengths, generated by both target and nontarget proteases, including metalloproteases, have been detected in human biological fluids and tissues. Beyond reflecting proteolytic activity, these peptides provide clinically relevant information on disease-associated inflammation and tissue remodeling. Accordingly, they are emerging as promising diagnostic, monitoring, and predictive biomarkers. Here, we summarize current knowledge on cleaved AAT fragments, their biological functions, and their potential clinical applications.