International immunopharmacology最新文献

{"title":"RBM15-mediated m6A methylation of Entpd1/CD39 regulates extracellular ATP hydrolysis and alleviates myocardial ischemia-reperfusion injury","authors":"Zhisheng Yan,&nbsp;Huihui Cao,&nbsp;Xiran Zhang,&nbsp;Yikang Wang,&nbsp;Qing Chang","doi":"10.1016/j.intimp.2025.115141","DOIUrl":"10.1016/j.intimp.2025.115141","url":null,"abstract":"<div><div>Myocardial ischemia-reperfusion (I/R) injury is a major cause of heart damage, linked to disrupted ATP metabolism and oxidative stress. While m6A RNA methylation regulates various cellular processes, its role in modulating I/R injury and ATP hydrolysis remains unclear. In this study, we demonstrate that both in vivo (rat I/R model) and in vitro (H/R-treated cardiomyocytes) models exhibit increased m6A modification levels during I/R injury. Among key m6A regulators, RBM15 is significantly upregulated in ischemic heart tissue. Functional assays reveal that RBM15 directly modulates the m6A methylation of Entpd1 (CD39), enhancing its expression and activity. Overexpression of RBM15 promotes ATP hydrolysis, resulting in increased adenosine production. These molecular changes collectively mitigated oxidative stress, reduced inflammation, and decreased apoptosis, resulting in improved cardiac function, smaller infarct sizes, and less cell death in the I/R model. These protective effects are reversed by CD39 inhibitor (sodium polyoxotungstate, POM-1), confirming the pivotal role of CD39 in this pathways. Mechanistically, RBM15 also activates the AMPK and AKT/ERK/GSK3β signaling pathway by increasing phosphorylation levels, further contributing to cardioprotection. In summary, RBM15-mediated m6A methylation enhances CD39 expression, facilitating extracellular ATP hydrolysis and exerting protective effects against myocardial I/R injury, highlighting its potential as a therapeutic target.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115141"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535029","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":"Artesunate promotes intestinal epithelial barrier repair by facilitating HMGCS2-dependent ketogenesis in experimental ulcerative colitis model mice","authors":"Guan Wang ,&nbsp;Lizhuang Han ,&nbsp;Haimei Sun ,&nbsp;Tingyi Sun ,&nbsp;Bo Wu ,&nbsp;Xu Cheng ,&nbsp;Shu Yang ,&nbsp;Deshan Zhou","doi":"10.1016/j.intimp.2025.115152","DOIUrl":"10.1016/j.intimp.2025.115152","url":null,"abstract":"<div><div>Ulcerative colitis (UC) is a chronic inflammatory disorder characterized by an impaired intestinal epithelial barrier. The complex etiology of UC includes genetic, environmental, immune and microbial factors. It has recently been proposed that dysregulated ketogenesis may play a role in the development of UC; however, the precise mechanism by which this occurs remains unclear. In this study, mice were treated with dextran sulfate sodium to induce UC. UC mice exhibited intestinal epithelial barrier dysfunction characterized by loss of tight junctions in intestinal epithelial cells (IECs) and an imbalance in the Th17/Treg ratio in the peripheral blood. A significant decrease in the ketogenic rate-limiting enzyme HMGCS2 was observed in the IECs of UC mice, which was responsible for the decrease of β-hydroxybutyric acid production. Notably, UC mice treated with artesunate (ART) showed increased HMGCS2 and ketogenesis, as well as restored Th17/Treg and recovered tight junction protein expression. These factors contributed to intestinal epithelial barrier repair and alleviated colitis. The addition of an AMPK inhibitor or mTOR activator effectively reversed the effects of ART on ketogenesis, thereby preventing subsequent restoration of the intestinal barrier. These findings were confirmed <em>in vitro</em> in DSS-treated colonocytes. In conclusion, ART facilitated intestinal epithelial barrier repair in UC by stimulating HMGCS2-dependent ketogenesis in IECs through the AMPK/mTOR signaling pathway.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115152"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535027","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":"Exosomal miR-3529-3p increases the sensitivity of trastuzumab via Wnt/β-catenin signaling pathway by targeting HOOK3","authors":"Junwen Zhu ,&nbsp;Ying Lu ,&nbsp;Qingyuan Zhang","doi":"10.1016/j.intimp.2025.115160","DOIUrl":"10.1016/j.intimp.2025.115160","url":null,"abstract":"<div><div>Trastuzumab is frequently utilized to treat human epidermal growth factor receptor 2 (HER2)-positive breast cancer, though its effectiveness is frequently hindered by the development of chemotherapy resistance. Recent research has indicated that exosomes, serving as carriers for genetic material exchanged among diverse tumor cell populations, contribute to the transmission of drug resistance, thereby promoting cancer progression. However, the exact mechanisms through which exosomes originating from breast cancer influence drug resistance remain unclear. In this study, we performed sequencing on exosomes both before and after trastuzumab treatment. Our results demonstrated a significant reduction in miR-3529-3p levels in exosomes from breast cancer patients following trastuzumab treatment compared to pre-treatment levels. Furthermore, miR-3529-3p was also downregulated in cells resistant to trastuzumab. Notably, overexpressing miR-3529-3p counteracted trastuzumab resistance. Additionally, miR-3529-3p mitigated chemoresistance by inhibiting the Wnt signaling pathway through positively regulating HOOK3 expression. In summary, miR-3529-3p in exosomes plays a crucial role in overcoming trastuzumab resistance, highlighting its potential as both a therapeutic target and a prognostic marker for individuals with breast cancer.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115160"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535030","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":"Apigenin alleviates dextran sulfate sodium-induced ulcerative colitis via regulation of endoplasmic reticulum stress in goblet cells","authors":"Zhong-Hao Ji ,&nbsp;Hai-Xiang Guo ,&nbsp;Bingbing Wang ,&nbsp;Wen-Zhi Ren ,&nbsp;Jin-Ping Hu ,&nbsp;Chengzhen Chen ,&nbsp;Bao Yuan","doi":"10.1016/j.intimp.2025.115164","DOIUrl":"10.1016/j.intimp.2025.115164","url":null,"abstract":"<div><div>Ulcerative colitis (UC) significantly impairs quality of life and incurs substantial economic costs. Apigenin, a flavonoid abundant in fruits and vegetables, has demonstrated potential in UC management. Utilizing DSS-induced UC mouse models and LS 174 T goblet cell models, this study elucidates apigenin's protective mechanisms. Dietary supplementation with 40 mg/kg apigenin markedly alleviated UC symptoms. Antibiotic-mediated microbiota depletion confirmed that apigenin's efficacy is independent of gut microbiota. Mechanistically, apigenin enhances SERCA2 expression to maintain intracellular calcium homeostasis, thereby inhibiting excessive activation of the PERK-eIF2α-ATF4-CHOP pathway, reducing goblet cell apoptosis, and preserving mucosal barrier integrity. These findings provide a robust theoretical foundation for apigenin as a dietary supplement in the prevention and mitigation of colitis.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115164"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535033","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":"Curcumin analogue C66 ameliorates the pathology of Alzheimer's disease through suppression of JNK signaling pathway","authors":"Li Xiong ,&nbsp;Qin Yu ,&nbsp;Linjie Chen ,&nbsp;Yu Deng ,&nbsp;Qi Ai ,&nbsp;Xiaoxia Xu ,&nbsp;Ziyao Meng ,&nbsp;Fan Chen ,&nbsp;Xia Zhao ,&nbsp;Jurui Wei ,&nbsp;Houming Yu","doi":"10.1016/j.intimp.2025.115156","DOIUrl":"10.1016/j.intimp.2025.115156","url":null,"abstract":"<div><div>Oxidative stress and neuroinflammation are two key pathological features in the early stage of Alzheimer's disease (AD), and they promote each other to further drive the progression of AD. Therefore, the development of therapeutic agents with dual anti-inflammatory and antioxidant properties represents a promising strategy for AD treatment. C66, a synthetic derivative of curcumin, protected PC12 cells and primary neurons from oxidative damage caused by Aβ. In addition, C66 alleviated Aβ-induced excessive inflammatory response in BV2 cells. Further results showed that C66 reduced neuroinflammation and neuronal apoptosis, ultimately improved cognitive decline in APPswe/PSEN1dE9 (APP/PS1) double transgenic AD mice. Importantly, C66 exhibited superior improved properties in APP/PS1 mice compared with the clinical control drug donepezil. Mechanistically, we indicated that C66 conferred its neuroprotective effects by inhibiting c-Jun N-terminal kinase (JNK) pathway. The result was further confirmed by using SP600125, a specific JNK inhibitor. Together, our findings suggest that C66 is expected to be further developed as a drug candidate for AD therapy.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115156"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535026","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":"Propionate alleviated colitis by modulating iron homeostasis to inhibit ferroptosis and macrophage polarization","authors":"Ting Yao ,&nbsp;Xiangmin Dong ,&nbsp;Jiawen Lv ,&nbsp;Liyun Fu ,&nbsp;Lanjuan Li","doi":"10.1016/j.intimp.2025.115151","DOIUrl":"10.1016/j.intimp.2025.115151","url":null,"abstract":"<div><div>Ulcerative colitis (UC) is a relapsing inflammatory bowel disease with limited effective treatment options. Ferroptosis, characterized by lipid peroxidation-induced cellular death, is involved in UC pathogenesis. Propionic acid, a short-chain fatty acid, has demonstrated therapeutic potential in alleviating numerous conditions; however, its role and underlying mechanisms in UC remain unclear. In this study, we analyzed ferroptosis in UC patients using datasets from the GEO database and established an experimental colitis model to evaluate the therapeutic effects of propionate. We assessed the markers of inflammation and ferroptosis. Our findings revealed that ferroptosis occurred in the colonic tissue of UC patients and mouse colitis model. Propionate effectively alleviated UC symptoms, reduced pro-inflammatory cytokines, and regulated iron homeostasis. At a dose of 100 mM, propionate promoted intestinal epithelial regeneration, while 400 mM inhibited ferroptosis significantly. Mechanistic studies demonstrated that propionate increased the expression of transferrin receptor 1 (TFR1) and ferritin heavy chain 1 (FTH1) in a dose-dependent manner, which was associated with reduced hypoxia-inducible factor 1α (HIF-1α) expression. Moreover, after inhibition of HIF-1α, the therapeutic effects of propionate on colonic symptoms were found to be similar. Furthermore, propionate promoted the polarization of macrophages to the M2 type. Our results indicate that propionate regulates HIF-mediated expression of TFR1 and FTH1 to modulate iron homeostasis, promote epithelial regeneration, inhibit ferroptosis, and regulate macrophage differentiation. These results strongly support the potential use of propionate in the clinical treatment of UC.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115151"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535032","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":"Innate immunity in the brain: ILC2s as modulators of CNS disorders","authors":"Jyotsna D. Godavarthi ,&nbsp;Anilkumar Pillai ,&nbsp;Rodrigo Morales ,&nbsp;Vijayasree V. Giridharan","doi":"10.1016/j.intimp.2025.115147","DOIUrl":"10.1016/j.intimp.2025.115147","url":null,"abstract":"<div><div>Innate lymphoid cells (ILCs), particularly group 2 innate lymphoid cells (ILC2s), have emerged as crucial players in central nervous system (CNS) homeostasis and pathology. This review explores the multifaceted roles of ILC2s across various CNS disorders, highlighting their potential as therapeutic targets. ILC2s, enriched in brain barriers like the meninges and choroid plexus, respond to alarmins such as IL-33 and IL-25, orchestrating immune responses through producing type 2 cytokines including IL-5 and IL-13. In aging brains, ILC2s demonstrate remarkable adaptability, resisting senescence, and maintaining self-renewal capacity. However, in Alzheimer's disease, ILC2s show numerical and functional deficits, potentially exacerbating neuroinflammation and cognitive decline. This review synthesizes recent findings on ILC2 involvement in CNS injuries, infections, stroke, ischemia, and their influence on behavior and cognition. We examine how ILC2s modulate neuroinflammation, promote tissue repair, and impact cognitive outcomes across these conditions. By integrating current research, we aim to provide a comprehensive understanding of ILC2 functions in CNS disorders and their potential as targets for novel therapeutic strategies.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115147"},"PeriodicalIF":4.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535028","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":"Pellitorine protects chronic restraint stress-induced cognitive deficits via inhibiting neural inflammation and ferroptosis","authors":"Jia-Bao Zhang ,&nbsp;Guo-Dong Lu ,&nbsp;Dan-Ni Sun ,&nbsp;Peng Ding ,&nbsp;Ya-Kun Chen ,&nbsp;Yan-Yan Zhou ,&nbsp;Yi-Ting Chen ,&nbsp;Mudan Cai ,&nbsp;Jong Hoon Ryu ,&nbsp;Pei Wang ,&nbsp;Yong-Ping Liang","doi":"10.1016/j.intimp.2025.115166","DOIUrl":"10.1016/j.intimp.2025.115166","url":null,"abstract":"<div><h3>Background</h3><div>It has not been known that pellitorine, an active ingredient of <em>Piper sarmentosum Roxb.</em> with therapeutic effects against epilepsy and anxiety disorders, has the neurological effects. Our study aimed to investigate the therapeutic potential of pellitorine in addressing chronic restraint stress (CRS)-associated cognitive deficits.</div></div><div><h3>Methods</h3><div>The CRS mouse model was treated with pellitorine and subjected to depression-like behavior assessments. Neuronal survival was evaluated through histological and Nissl staining. Immunoblotting assays were conducted to examine the expression levels of signaling pathway proteins. Immunofluorescent staining, flow cytometry, and RNA sequencing were utilized to further elucidate the pathological and molecular changes in pellitorine-treated CRS mice.</div></div><div><h3>Results</h3><div>Behavioral experiments demonstrated that pellitorine treatment significantly alleviated depression-like behaviors and improved cognitive function in CRS mice. Histological analysis revealed a marked reduction in neuronal loss following pellitorine administration. Transcriptomic profiling indicated that pellitorine suppressed ferroptosis-associated signaling pathways and neuroinflammation. Notably, the expression of anti-ferroptosis factors, including GPX4, DHODH, and FSP1, was decreased in CRS mice but restored by pellitorine treatment. In addition, pellitorine prevented neuronal loss, preserved the expression of neuroprotective molecules such as BDNF, Nrf2, HO-1, phosphorylated-CREB, and phosphorylated-ERK1/2, and reduced the protein levels of inflammation-related markers including NLRP3, HMGB1, and NF-κB. Immunofluorescent staining and flow cytometry analyses further showed that pellitorine treatment reduced the number of activated microglia, as indicated by decreased Iba-1⁺, TREM2⁺, CD86⁺, and CX3CR1⁺ cell populations in the hippocampus. Importantly, pellitorine did not exhibit any observable neurotoxic effects in healthy control mice.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that pellitorine protects against CRS-induced cognitive deficits, neural inflammation, and ferroptosis, highlighting its promise as a therapeutic agent for mental health issues.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115166"},"PeriodicalIF":4.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535031","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":"Targeting NEK7 modulates pyroptosis and gut microbiota to alleviate depression-like behavior in rats","authors":"Wenxuan Lang ,&nbsp;Chongji Wang ,&nbsp;Jiahui Wen ,&nbsp;Miaoqi Chen ,&nbsp;Decheng Wei ,&nbsp;Yanzong Jiang ,&nbsp;Xue Li ,&nbsp;Pengsheng Wei ,&nbsp;Ge Jin ,&nbsp;Qiwen Zhu","doi":"10.1016/j.intimp.2025.115148","DOIUrl":"10.1016/j.intimp.2025.115148","url":null,"abstract":"<div><div>NIMA-associated kinase 7 (NEK7) is a serine/threonine kinase that regulates the aberrant activation of the inflammasome of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), which leads to inflammatory diseases. Depression, a prevalent psychiatric condition, has been linked to neuroinflammatory processes. However, the precise molecular and cellular mechanisms underlying the role of NEK7 in depression pathogenesis remain incompletely characterized. Our study demonstrated elevated NEK7 expression in the hippocampus of maternal separation (MS) and chronic unpredictable mild stress (CUMS)-induced depressed rats. Adeno-associated virus (AAV)-mediated delivery of shNEK7 effectively alleviated depression-like behavioral deficits, downregulated pyroptosis marker protein expression, reduced inflammatory cytokine levels (interleukin-1β and interleukin-18), and preserved neuronal survival and cellular structure. Furthermore, hippocampal NEK7 knockdown restored gut microbiota homeostasis in depression-like rats, particularly affecting the relative abundance of <em>Corynebacterium</em> and <em>Prevotella</em> genera. Notably, for the first time, the metabolite corynoxine was found to be associated with hippocampal NEK7 knockdown in depression-like rats. Taken together, our results reveal that NEK7 may be a promising target for the treatment of depression and provide new experimental evidence for clinical application.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115148"},"PeriodicalIF":4.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144523222","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":"MIA and CD163 as promising diagnostic biomarkers in vascular dementia: A multi-method study combining WGCNA, machine learning with validation in animal models and clinical samples","authors":"Yun-meng Chen ,&nbsp;Ze Chang ,&nbsp;Xiao Liang,&nbsp;Li-na Miao,&nbsp;Xian-su Chi,&nbsp;Hong-xi Liu,&nbsp;Wei Shen,&nbsp;Yun-ling Zhang","doi":"10.1016/j.intimp.2025.115146","DOIUrl":"10.1016/j.intimp.2025.115146","url":null,"abstract":"<div><div>Vascular dementia (VaD), the second most common form of dementia, lacks reliable biomarkers for early diagnosis. Here, we integrated weighted gene co-expression network analysis (WGCNA) with machine learning to identify novel biomarkers and immune-metabolic pathways in VaD. Analysis of the GSE122063 dataset revealed 288 differentially expressed genes (DEGs), with four hub genes (MIA, CD163, OPALIN, SNX31) prioritized by LASSO regression and Random Forest. A nomogram model incorporating these genes achieved an AUC of 0.924, demonstrating high diagnostic accuracy. External validation (GSE186798) and experimental studies confirmed significant upregulation of MIA and CD163 in VaD patients and a 2VO rat model (<em>P</em> &lt; 0.05), while SNX31 and OPALIN showed inconsistent significance. Mechanistically, MIA and CD163 correlated with macrophage polarization (M1/M2) and dysregulated oxidative phosphorylation pathways, suggesting their dual roles in neuroinflammation and metabolic reprogramming. Serum ELISA further validated elevated MIA (14.34 ± 6.32 vs. 5.23 ± 4.89 ng/mL) and CD163 (141.31 ± 71.27 vs. 58.09 ± 54.31 ng/mL) in VaD patients (<em>P</em> &lt; 0.05). Our study not only establishes MIA and CD163 as robust diagnostic biomarkers but also highlights their potential as therapeutic targets for modulating immune-metabolic crosstalk in VaD pathogenesis.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"162 ","pages":"Article 115146"},"PeriodicalIF":4.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144523223","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}