International immunopharmacology最新文献_第10页

A small-molecule enhancer of STAT1 affects herpes simplex keratitis prognosis by mediating plasmacytoid dendritic cells migration through CXCR3/CXCL10 STAT1的小分子增强子通过CXCR3/CXCL10介导浆细胞样树突状细胞迁移影响单纯疱疹性角膜炎的预后。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.113959

Yujin Wang , Jiewen Mao , Kuiliang Yang , Qian Deng , Yuelan Gao , Yulin Yan , Zixian Yang , Yuyu cong , Shanshan Wan , Wanju Yang , Yanning Yang

{"title":"A small-molecule enhancer of STAT1 affects herpes simplex keratitis prognosis by mediating plasmacytoid dendritic cells migration through CXCR3/CXCL10","authors":"Yujin Wang , Jiewen Mao , Kuiliang Yang , Qian Deng , Yuelan Gao , Yulin Yan , Zixian Yang , Yuyu cong , Shanshan Wan , Wanju Yang , Yanning Yang","doi":"10.1016/j.intimp.2024.113959","DOIUrl":"10.1016/j.intimp.2024.113959","url":null,"abstract":"<div><div>Herpes simplex keratitis (HSK) is a prevalent infectious corneal disorder. This study aims to explore the role of plasmacytoid dendritic cells (pDCs) in HSK, an area that remains underexplored. The investigation centers on the effects of a STAT1 transcription enhancer, 2-NP, on pDCs and its underlying mechanisms. Our findings revealed that 2-NP treatment significantly reduced corneal opacity and neovascularization in a mouse HSK model. This intervention increased CXCR3 expression on the cell membrane, promoting pDC migration to the cornea <em>via</em> the CXCR3/CXCL10 axis. Additionally, it triggered STAT1 phosphorylation, enhancing IFN-α production, which in turn activated the JAK1/STAT1 signaling pathway. These results uncover a novel molecular mechanism by which the STAT1 transcriptional enhancer drives pDC migration to inflamed corneas, presenting a new therapeutic strategy for HSK.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 113959"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927109","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}

引用次数: 0

Kaempferol attenuates experimental autoimmune neuritis through TNFR1/JNK/p38 signaling pathway inhibition 山奈酚通过抑制TNFR1/JNK/p38信号通路减轻实验性自身免疫性神经炎。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.113951

Li Wang , Tao Gu , Chunguang Yu , Yingying Gao , Tingting Xuan , Kaichun Shen , Guowei Wang , Zhenhai Wang

{"title":"Kaempferol attenuates experimental autoimmune neuritis through TNFR1/JNK/p38 signaling pathway inhibition","authors":"Li Wang , Tao Gu , Chunguang Yu , Yingying Gao , Tingting Xuan , Kaichun Shen , Guowei Wang , Zhenhai Wang","doi":"10.1016/j.intimp.2024.113951","DOIUrl":"10.1016/j.intimp.2024.113951","url":null,"abstract":"<div><div>Kaempferol (Kae) is a flavonoid that has antioxidant, anti-inflammatory and neuroprotective effects. In recent years, there have been increasing reports on viral infection-induced Guillain-Barré syndrome (GBS) with high rates of disability and fatality. Therefore, in order to search for effective peripheral nerve injury repair drugs, we used rats with experimental autoimmune neuritis (EAN) as the typical animal model for GBS, and implemented Kae treatment intervention on EAN rats. Real-time quantitative polymerase chain reaction (qPCR), western blotting (WB) and immunofluorescence (IF) were utilized to detect the changes of inflammatory factors and signaling pathway proteins in peripheral nerve of rats. The impact of Kae on peripheral nerve damage in EAN rats was evaluated in multiple dimensions by clinical symptom score and neuroelectrophysiology examination, and the protective impact and mechanism of Kae on peripheral nerve injury were revealed. Our results showed that Kae increased the expression of sciatic myelin basic protein (MBP), decreased the expression of peripheral nerve macrophage infiltration and inflammatory cytokines, including TNF-α, IL-1β and IL-6, and down-regulated the expression levels of TNFR1. Additionally, it suppressed the activation of the JNK and p38 pathways. It can alleviate sciatic nerve symptoms and pathological injury in EAN rats. Therefore, we believe that Kae can be used as an adjunct drug in the treatment of GBS.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 113951"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927234","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}

引用次数: 0

Brucella abortus transcriptional regulator ArsR6 inhibits host pyroptosis via BAB_RS28760 by triggering the endoplasmic reticulum stress pathway 流产布鲁氏菌转录调节因子ArsR6通过触发内质网应激途径，通过BAB_RS28760抑制宿主热亡。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.114001

Dexin Zhu , Jia Guo , Xingmei Deng , Min Li , Yong Wang , Zhen Wang , Zhihua Sun , Shuzhu Cao , Tianyi Zhao , Yimei Xu , Liangbo Liu , Hui Zhang

{"title":"Brucella abortus transcriptional regulator ArsR6 inhibits host pyroptosis via BAB_RS28760 by triggering the endoplasmic reticulum stress pathway","authors":"Dexin Zhu , Jia Guo , Xingmei Deng , Min Li , Yong Wang , Zhen Wang , Zhihua Sun , Shuzhu Cao , Tianyi Zhao , Yimei Xu , Liangbo Liu , Hui Zhang","doi":"10.1016/j.intimp.2024.114001","DOIUrl":"10.1016/j.intimp.2024.114001","url":null,"abstract":"<div><div>Pyroptosis, which is accompanied by inflammatory responses, is critical for pathogen clearance. However, the mechanism through which <em>Brucella</em> evades host pyroptosis remains unclear. The transcriptional regulator ArsR6 maintains bacterial intracellular homeostasis and possibly influences host cell death. However, whether ArsR6 acts on cellular pyroptosis is unknown. Therefore, we investigated pathogen-host interactions within macrophages infected with <em>Brucella abortus</em> (<em>B. abortus</em>), and found that ArsR6 is crucial for inhibiting host cell pyroptosis after <em>B. abortus</em> infection. The downstream target gene, <em>BAB_RS28760</em> of ArsR6 was screened using chromatin immunoprecipitation sequencing. BAB_RS28760 belongs to the BA14K protein family and is strongly immunoreactive and induces humoral and cellular immune responses in the host during infection. Deleting ArsR6 in <em>B. abortus<!--> </em>promotes pyroptosis and enhancs the intracellular survival of <em>B. abortus</em>. In addition, ArsR6 negatively regulated its target gene <em>BAB_RS28760</em>, whereas BAB_RS28760 deletion downregulated cellular pyroptosis by inhibiting endoplasmic reticulum stress and decreasing the intracellular survival of <em>B. abortus</em>. Our results reveal for the first time that <em>Brucella</em> ArsR6 reduces endoplasmic reticulum stress activation by negatively regulating its downstream target genes, thus inhibiting host cell pyroptosis. Our study provides new insights into the pathogenic mechanisms of <em>Brucella</em>, which can provide potential selectivity for the development of anti-<em>Brucella</em> therapies.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 114001"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947875","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}

引用次数: 0

Electroacupuncture normalized tumor vasculature by downregulating glyoxalase-1 to polarize tumor-associated macrophage to M1 phenotype in triple-negative breast cancer 在三阴性乳腺癌中，电针通过下调乙二醛酶-1使肿瘤相关巨噬细胞极化为M1表型而使肿瘤血管正常化。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.113988

Xuewei Qi , Yanyan Lian , Zhenjia Fan , Hui Wang , Honglin Jiang , Mengyang He , Liling Li , Jinchang Huang , Yuxiang Wan

{"title":"Electroacupuncture normalized tumor vasculature by downregulating glyoxalase-1 to polarize tumor-associated macrophage to M1 phenotype in triple-negative breast cancer","authors":"Xuewei Qi , Yanyan Lian , Zhenjia Fan , Hui Wang , Honglin Jiang , Mengyang He , Liling Li , Jinchang Huang , Yuxiang Wan","doi":"10.1016/j.intimp.2024.113988","DOIUrl":"10.1016/j.intimp.2024.113988","url":null,"abstract":"<div><h3>Background</h3><div>Triple-negative breast cancer is a particularly aggressive type of breast cancer that is closely associated with abnormal vascularization within the tumor. However, traditional anti-VEGF therapies and other treatments have limited efficacy. Tumor-associated macrophages (TAMs) induce and regulate tumor angiogenesis. In recent years, regulating TAMs polarization has become a hot topic for research with objectives to normalize tumor vasculature and improve drug delivery and the tumor microenvironment. Our previous studies have found that peritumoral electroacupuncture (EA) can regulate tumor angiogenesis, but the underlying mechanism remains unclear.</div></div><div><h3>Methods</h3><div>In this study, we examined the phenotype of TAMs and inflammatory factors to observe the effect of peritumoral electroacupuncture on the phenotypic polarization of TAMs. Based on this, we evaluated the structure and function of tumor vasculature. Finally, we conducted a preliminary exploration of the mechanism underlying the regulation of TAMs phenotypic polarization by peritumoral electroacupuncture.</div></div><div><h3>Results</h3><div>In this study, we found that peritumoral electroacupuncture could promote the phenotypic polarization of TAMs toward the M1 type, thereby reducing microvascular density in tumor tissue, increasing pericyte coverage, improving the stability of the basement membrane, promoting vascular maturation, and enhancing perfusion while reducing tissue hypoxia.</div></div><div><h3>Conclusions</h3><div>Peritumoral electroacupuncture can promote the phenotypic polarization of TAMs toward the M1 type, leading to normalization of tumor vascular structure and function. The mechanism may be related to the downregulation of glyoxalase-1 and subsequent activation of the MGO-AGEs/RAGE axis.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 113988"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948098","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}

引用次数: 0

Canthaxanthin ameliorates atopic dermatitis in mice by suppressing Th2 immune response. 角黄素通过抑制Th2免疫反应改善小鼠特应性皮炎。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 Epub Date: 2025-01-08 DOI: 10.1016/j.intimp.2024.113975

Shuying Peng, Lu Yu, Mingxin Jiang, Sihang Cao, Hong Wang, Xiao Lu, Yihao Tao, Jia Zhou, Ledong Sun, Daming Zuo

{"title":"Canthaxanthin ameliorates atopic dermatitis in mice by suppressing Th2 immune response.","authors":"Shuying Peng, Lu Yu, Mingxin Jiang, Sihang Cao, Hong Wang, Xiao Lu, Yihao Tao, Jia Zhou, Ledong Sun, Daming Zuo","doi":"10.1016/j.intimp.2024.113975","DOIUrl":"10.1016/j.intimp.2024.113975","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder characterized by intense pruritus and complex immunopathogenic mechanisms. Recent evidence has highlighted the critical link between dysregulated intestinal microecology and altered immune responses in AD progression. As essential components of the intestinal microenvironment, metabolites play pivotal roles in various physiological processes. Through metabolomic profiling in an AD mouse model, we identified a significant reduction in canthaxanthin (CTX), a bacterial-derived metabolite naturally present in many foods, in AD mice compared to healthy controls. To investigate the therapeutic potential of CTX, we established an AD model by repeatedly applying 2,4-dinitrochlorobenzene (DNCB) to the ears and dorsal skin of mice, successfully inducing AD-like symptoms and lesions. Notably, oral administration of CTX significantly attenuated skin inflammation and reduced serum IgE levels in this DNCB-induced AD model. Both in vivo and in vitro studies demonstrated that CTX treatment effectively suppressed Th2 immune responses. Mechanistically, we found that CTX significantly inhibited the activation of the JAK2-STAT6 signaling pathway in Th2-polarized T cells. Our findings not only demonstrate the therapeutic efficacy of CTX in AD but also elucidate its molecular mechanism in modulating T helper cell subset balance. These insights suggest that CTX could serve as a promising therapeutic agent for AD and potentially other Th2 response-mediated immune disorders.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"113975"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947973","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}

引用次数: 0

Role of TRIM29 in disease: What is and is not known TRIM29在疾病中的作用：已知的和未知的。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.113983

Kunying Lv , Qilong Li , Ning Jiang , Qijun Chen

{"title":"Role of TRIM29 in disease: What is and is not known","authors":"Kunying Lv , Qilong Li , Ning Jiang , Qijun Chen","doi":"10.1016/j.intimp.2024.113983","DOIUrl":"10.1016/j.intimp.2024.113983","url":null,"abstract":"<div><div>Tripartite motif-containing proteins (TRIMs), comprising the greatest subfamily of E3 ubiquitin ligases with approximately 80 members of this family, are widely distributed in mammalian cells. TRIMs actively participate in ubiquitination of target proteins, a type of post-translational modification associated with protein degradation and other functions. Tripartite motif-containing protein 29 (TRIM29), a member of the TRIM family, differs from other members of this family in that it lacks the RING finger structural domain containing cysteine and histidine residues that mediates DNA binding, protein–protein interactions, and ubiquitin ligase, at its N-terminus. The expression of TRIM29 was initially found to be associated with cancer and diabetic nephropathy progression, and antiviral immunity which is triggered by virus-derived nucleic acids binding to pattern recognition receptors (PRRs) on immune cells. Recently, TRIM29 has also been explored as a diagnostic biomarker and therapeutic target for some immune-related diseases. Here, we review the functions of TRIM29 in the progression of diseases and the inherent mechanisms, as well as the remaining gaps in the literature. A thorough understanding of the detailed regulatory mechanisms of TRIM29 will ultimately facilitate the development of different therapeutic strategies for various diseases.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 113983"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925923","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}

引用次数: 0

Bafilomycin A1 mitigates subchondral bone degeneration and pain in TMJOA rats 巴菲霉素A1减轻TMJOA大鼠软骨下骨变性和疼痛。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 DOI: 10.1016/j.intimp.2024.113947

Henghua Jiang , Wei Fang , Yaping Feng , Xin Liu , Jie Zhao , Liqin Xu , Guangli Han , Xing Long

{"title":"Bafilomycin A1 mitigates subchondral bone degeneration and pain in TMJOA rats","authors":"Henghua Jiang , Wei Fang , Yaping Feng , Xin Liu , Jie Zhao , Liqin Xu , Guangli Han , Xing Long","doi":"10.1016/j.intimp.2024.113947","DOIUrl":"10.1016/j.intimp.2024.113947","url":null,"abstract":"<div><h3>Background</h3><div>Pain and disability are primary concerns for temporomandibular joint osteoarthritis (TMJOA) patients, and the efficacy of current treatments remains controversial. Overactive osteoclasts are associated with subchondral bone degeneration and pain in OA. The vacuolar H+-ATPase (V-ATPase) is crucial for differentiation and function in osteoclasts, but its role in TMJOA is not well defined. This study aims to evaluate the effects of the V-ATPase inhibitor, bafilomycin A1 (Baf A1) on the progression and pain of TMJOA.</div></div><div><h3>Materials and methods</h3><div>Pain behavior tests, histological staining, tartrate-resistant acid phosphatase (TRAP) staining, immunofluorescence staining, and micro-CT analysis were conducted to evaluate the therapeutic efficacy of Baf A1 in monosodium iodoacetate-induced TMJOA in rats. Additionally, TRAP staining, enzyme-linked immunosorbent assay and immunofluorescence staining were used to assess the inhibitory effects of Baf a1 on the osteoclastogenesis, secretion of netrin-1 and neurite growth of trigeminal ganglion (TG) neurons.</div></div><div><h3>Results</h3><div>Baf A1 significantly mitigated subchondral bone degeneration by suppressing osteoclastogenesis and subsequently inhibited cartilage degradation in TMJOA rats. Baf A1 also effectively alleviated pain behavior by inhibiting expression of netrin-1 and innervation of sensory nerve in TMJOA rats. In vitro assays of osteoclast and TG further demonstrated the inhibitory effects of Baf A1 on osteoclastogenesis, secretion of netrin-1 and neurite outgrowth of TG.</div></div><div><h3>Conclusions</h3><div>This study demonstrates that Baf A1 inhibits V-ATPase to mitigate TMJOA degeneration and pain by suppressing osteoclastogenesis and secretion of netrin-1, thereby suggesting it as a potential clinical treatment option for degeneration and pain of TMJOA.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"Article 113947"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931600","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}

引用次数: 0

Targeting the tumor immune microenvironment: GPCRs as key regulators in triple-negative breast cancer. 靶向肿瘤免疫微环境：gpcr在三阴性乳腺癌中的关键调控作用

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 Epub Date: 2024-12-30 DOI: 10.1016/j.intimp.2024.113930

Chengyi Wang, Yanyan Liu, Ru Zhang, Hao Gong, Xinnong Jiang, Shuai Xia

{"title":"Targeting the tumor immune microenvironment: GPCRs as key regulators in triple-negative breast cancer.","authors":"Chengyi Wang, Yanyan Liu, Ru Zhang, Hao Gong, Xinnong Jiang, Shuai Xia","doi":"10.1016/j.intimp.2024.113930","DOIUrl":"10.1016/j.intimp.2024.113930","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) poses a significant clinical challenge due to its aggressive nature and limited therapeutic options. Recent research underscores the pivotal role of G protein-coupled receptors (GPCRs) in shaping the tumor immune microenvironment (TIME) within TNBC. This review focuses on four principal GPCRs-chemokine receptors, sphingosine-1-phosphate receptors, prostaglandin E2 receptors, and lactate receptors-that have garnered substantial attention in TNBC studies. GPCRs modulate immune cell recruitment, polarization, and function, thereby fostering an immunosuppressive milieu conducive to tumor progression and metastasis. The review examines how alterations in GPCR expression on immune cells influence the pathogenesis and advancement of TNBC. Further, it discusses emerging therapeutic strategies targeting GPCR signaling pathways to remodel the immunosuppressive TIME in TNBC. These insights into GPCR-mediated immune regulation not only deepen our comprehension of TNBC's pathophysiology but also offer promising avenues for developing novel immunotherapies aimed at enhancing clinical outcomes for TNBC patients.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"147 ","pages":"113930"},"PeriodicalIF":4.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909567","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}

引用次数: 0

Corrigendum to "SIRT6 knockdown alleviates keratinocyte hyperproliferation and inflammation in psoriasis via modulating acetylation of FOXO1" [Int. Immunopharmacol. 146 (2024) 113932]. “SIRT6敲低通过调节fox01乙酰化减轻银屑病角质细胞过度增殖和炎症”的更正[j]。中国生物医学工程学报，2014(5):349 - 349。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 Epub Date: 2025-01-10 DOI: 10.1016/j.intimp.2025.114066

Chuantao Cheng, Yuan Wang, Jia Huo, Yanfei Zhang, Ruilian Li

引用次数: 0

Corrigendum to "The SP1/SIRT1/ACLY signaling axis mediates fatty acid oxidation in renal ischemia-reperfusion-induced renal fibrosis" [Int. Immunopharmacol. 132 (2024) 112002]. “SP1/SIRT1/ACLY信号轴介导肾缺血-再灌注诱导的肾纤维化中脂肪酸氧化”的更正[j]。免疫药理，132(2024)112002。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-02-06 Epub Date: 2025-01-10 DOI: 10.1016/j.intimp.2024.113963

Huailiang Wu, Liyan Wang, Peng Kang, Xiangjun Zhou, Wei Li, Zhongyuan Xia

引用次数: 0