Inflammation最新文献_第6页

Targeting S100A12 to Improve Angiogenesis and Accelerate Diabetic Wound Healing. 靶向 S100A12 改善血管生成并加速糖尿病伤口愈合

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-02 DOI: 10.1007/s10753-024-02073-8

Shitian Qin, Fan Bie, Shuying Chen, Yingbin Xu, Lei Chen, Bin Shu, Fan Yang, Yangzhou Lu, Jialin Li, Jingling Zhao

{"title":"Targeting S100A12 to Improve Angiogenesis and Accelerate Diabetic Wound Healing.","authors":"Shitian Qin, Fan Bie, Shuying Chen, Yingbin Xu, Lei Chen, Bin Shu, Fan Yang, Yangzhou Lu, Jialin Li, Jingling Zhao","doi":"10.1007/s10753-024-02073-8","DOIUrl":"10.1007/s10753-024-02073-8","url":null,"abstract":"Long-term inflammation and impaired angiogenesis are thought to be the causes of delayed healing or nonhealing of diabetic wounds. S100A12 is an essential pro-inflammatory factor involved in inflammatory reactions and serves as a biomarker for various inflammatory diseases. However, whether high level of S100A12 exists in and affects the healing of diabetic wounds, as well as the underlying molecular mechanisms, remain unclear. In this study, we found that the serum concentration of S100A12 is significantly elevated in patients with type 2 diabetes. Exposure of stratified epidermal cells to high glucose environment led to increased expression and secretion of S100A12, resulting in impaired endothelial function by binding to the advanced glycation endproducts (RAGE) or Toll-like receptor 4 (TLR4) on endothelial cell. The transcription factor Krüpple-like Factor 5 (KLF5) is highly expressed in the epidermis under high glucose conditions, activating the transcriptional activity of the S100A12 and boost its expression. By establishing diabetic wounds model in alloxan-induced diabetic rabbit, we found that local inhibition of S100A12 significantly accelerated diabetic wound healing by promoting angiogenesis. Our results illustrated the novel endothelial-specific injury function of S100A12 in diabetic wounds and suggest that S100A12 is a potential target for the treatment of diabetic wounds.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"633-648"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491826","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

YTHDF2 Regulates Advanced Glycation End Products-Induced Melanogenesis through Inhibiting A20 Expression in Human Dermal Fibroblasts. YTHDF2通过抑制人真皮成纤维细胞中A20的表达来调节高级糖化终产物诱导的黑色素生成

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-16 DOI: 10.1007/s10753-024-02097-0

Jingjing Lan, Xianyin Huang, Hongpeng Li, Shen Lin, Jingqian Huang, Weixin Yang, Mengting Ouyang, Jiaqi Fang, Qingfang Xu

{"title":"YTHDF2 Regulates Advanced Glycation End Products-Induced Melanogenesis through Inhibiting A20 Expression in Human Dermal Fibroblasts.","authors":"Jingjing Lan, Xianyin Huang, Hongpeng Li, Shen Lin, Jingqian Huang, Weixin Yang, Mengting Ouyang, Jiaqi Fang, Qingfang Xu","doi":"10.1007/s10753-024-02097-0","DOIUrl":"10.1007/s10753-024-02097-0","url":null,"abstract":"Fibroblast A20 suppresses advanced glycation end products (AGEs)-induced melanogenesis by inhibiting NLRP3 inflammasome activation. AGEs repress A20 expression and significantly m6A-methylate A20 mRNA in fibroblasts. YTHDF2 is the most studied m6A reader protein and can accelerate degradation of m6A-modified mRNA. Whether YTHDF2 regulates AGEs-induced A20 expression and pigmentation is unknown. In this study, we confirmed that YTHDF2 inversely regulated AGEs-BSA-inhibited A20 expression but facilitated AGEs-BSA-activated NF-κB signaling and NLRP3 inflammasome in fibroblasts via YTHDF2 knockdown and overexpression experiments. Mechanistically, YTHDF2 bound to m6A-modified A20 mRNA induced by AGEs-BSA and increased its degradation. Moreover, fibroblast YTHDF2 robustly promoted AGEs-BSA-induced IL-18 level in coculture supernatants and melanin content, tyrosinase activity, and expression of microphthalmia-associated transcription factor and tyrosinase in melanocytes, which were significantly blocked by IL-18 binding protein. Further, fibroblast YTHDF2 markedly increased AGEs-BSA-induced epidermal melanin level in cocultured ex vivo skin and MAPKs activation in melanocytes. Importantly, upregulated dermal YTHDF2 expression was negatively correlated with dermal A20 level and positively associated with both epidermal melanin and dermal AGEs content in sun-exposed skin and lesions of melasma and solar lentigo. These findings suggest that fibroblast YTHDF2 positively regulates AGEs-induced melanogenesis mainly via A20/ NF-κB /NLRP3 inflammasome/ IL-18 /MAPKs axis in an m6A-dependent manner and functions in photoaging-induced hyperpigmentation skin disorders.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"919-934"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619805","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

Deciphering Autoimmune Diseases: Unveiling the Diagnostic, Therapeutic, and Prognostic Potential of Immune Repertoire Sequencing. 解密自身免疫性疾病：揭示免疫汇聚测序的诊断、治疗和预后潜力。

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-06-25 DOI: 10.1007/s10753-024-02079-2

Yuelin Hu, Jialing Huang, Shuqing Wang, Xin Sun, Xin Wang, Hongsong Yu

引用次数: 0

Monensin Suppresses Multiple Features of House Dust Mite-Induced Experimental Asthma in Mice. 莫能菌素可抑制屋尘螨诱发的小鼠实验性哮喘的多种特征

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-03 DOI: 10.1007/s10753-024-02090-7

Venkata Sita Rama Raju Allam, Srinivas Akula, Ida Waern, Sowsan Taha, Sara Wernersson, Gunnar Pejler

{"title":"Monensin Suppresses Multiple Features of House Dust Mite-Induced Experimental Asthma in Mice.","authors":"Venkata Sita Rama Raju Allam, Srinivas Akula, Ida Waern, Sowsan Taha, Sara Wernersson, Gunnar Pejler","doi":"10.1007/s10753-024-02090-7","DOIUrl":"10.1007/s10753-024-02090-7","url":null,"abstract":"Despite intense efforts to develop efficient therapeutic regimes for asthma, there is a large demand for novel treatment strategies in this disease. Here we evaluated the impact of monensin, a drug with potent anti-mast cell effects, in a mouse model of asthma. Allergic airway inflammation was induced by sensitization of mice with house dust mite (HDM) antigen, and effects of monensin on airway hyperreactivity and inflammatory parameters were studied. Following intraperitoneal administration, monensin did not suppress airway hyperreactivity but was shown to have anti-inflammatory properties, as manifested by reduced eosinophil- and lymphocyte infiltration into the airway lumen, and by suppressed inflammation of the lung tissue. After intranasal instillation, monensin exhibited similar anti-inflammatory effects as seen after intraperitoneal administration. Moreover, intranasally administered monensin was demonstrated to suppress goblet cell hyperplasia, and to cause a reduction in the expression of genes coding for key inflammatory markers. Further, monensin blocked mast cell degranulation in the airways of allergen-sensitized mice. Together, this study reveals that monensin has the capacity to suppress key pathological events associated with allergic airway inflammation.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"806-819"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491824","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

The Role of Cobalamin in Multiple Sclerosis: An Update. 钴胺素在多发性硬化症中的作用：最新进展。

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-06-21 DOI: 10.1007/s10753-024-02075-6

Marjan Golabi, Danial Kazemi, Amir Shayan Chadeganipour, Hamed Fouladseresht, Mark J M Sullman, Behrooz Ghezelbash, Ava Yeganegi Dastgerdi, Nahid Eskandari

引用次数: 0

Retraction Note: The Association of Cigarette Smoke Exposure with Lung Cellular Toxicity and Oxidative Stress: the Protective Role of Crocin. 撤稿说明：卷烟烟雾暴露与肺细胞毒性和氧化应激的关系：克罗霉素的保护作用。

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 DOI: 10.1007/s10753-024-02087-2

Maryam Radan, Mahin Dianat, Mohammad Badavi, Seyyed Ali Mard, Vahid Bayati, Masoumeh Ahmadizadeh

引用次数: 0

Ginkgolide C attenuated Western diet-induced non-alcoholic fatty liver disease via increasing AMPK activation. 银杏内酯C通过增加AMPK活化减轻了西方饮食引起的非酒精性脂肪肝。

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-01 DOI: 10.1007/s10753-024-02086-3

Yao Xie, Leyi Wei, Jiashi Guo, Qingsong Jiang, Yang Xiang, Yan Lin, Huang Xie, Xinru Yin, Xia Gong, Jingyuan Wan

{"title":"Ginkgolide C attenuated Western diet-induced non-alcoholic fatty liver disease via increasing AMPK activation.","authors":"Yao Xie, Leyi Wei, Jiashi Guo, Qingsong Jiang, Yang Xiang, Yan Lin, Huang Xie, Xinru Yin, Xia Gong, Jingyuan Wan","doi":"10.1007/s10753-024-02086-3","DOIUrl":"10.1007/s10753-024-02086-3","url":null,"abstract":"Background: Non-alcoholic steatohepatitis (NASH) is a metabolic dysregulation-related disorder that is generally characterized by lipid metabolism dysfunction and an excessive inflammatory response. Currently, there are no authorized pharmacological interventions specifically designed to manage NASH. It has been reported that Ginkgolide C exhibits anti-inflammatory effects and modulates lipid metabolism. However, the impact and function of Ginkgolide C in diet-induced NASH are unclear.Methods: In this study, mice were induced by a Western Diet (WD) with different doses of Ginkgolide C with or without Compound C (adenosine 5 '-monophosphate (AMP)-activated protein kinase (AMPK) inhibitor). The effects of Ginkgolide C were evaluated by assessing liver damage, steatosis, fibrosis, and AMPK expression.Results: The results showed that Ginkgolide C significantly alleviated liver damage, steatosis, and fibrosis in the WD-induced mice. In addition, Ginkgolide C markedly improved insulin resistance and attenuated hepatic inflammation. Importantly, Ginkgolide C exerted protective effects by activating the AMPK signaling pathway, which was reversed by AMPK inhibition.Conclusion: Ginkgolide C alleviated NASH induced by WD in mice, potentially via activating the AMPK signaling pathway.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"770-782"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491823","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

OTUD1 Deficiency Alleviates LPS-Induced Acute Lung Injury in Mice by Reducing Inflammatory Response. 缺失 OTUD1 可通过降低炎症反应缓解 LPS 诱导的小鼠急性肺损伤

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-22 DOI: 10.1007/s10753-024-02074-7

Weiwei Zhu, Qianhui Zhang, Leiming Jin, Shuaijie Lou, Jiaxi Ye, Yaqian Cui, Yongqiang Xiong, Mengsha Lin, Guang Liang, Wu Luo, Zaishou Zhuang

{"title":"OTUD1 Deficiency Alleviates LPS-Induced Acute Lung Injury in Mice by Reducing Inflammatory Response.","authors":"Weiwei Zhu, Qianhui Zhang, Leiming Jin, Shuaijie Lou, Jiaxi Ye, Yaqian Cui, Yongqiang Xiong, Mengsha Lin, Guang Liang, Wu Luo, Zaishou Zhuang","doi":"10.1007/s10753-024-02074-7","DOIUrl":"10.1007/s10753-024-02074-7","url":null,"abstract":"The ovarian tumor (OTU) family consists of deubiquitinating enzymes thought to play a crucial role in immunity. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) pose substantial clinical challenges due to severe respiratory complications and high mortality resulting from uncontrolled inflammation. Despite this, no study has explored the potential link between the OTU family and ALI/ARDS. Using publicly available high-throughput data, 14 OTUs were screened in a simulating bacteria- or LPS-induced ALI model. Subsequently, gene knockout mice and transcriptome sequencing were employed to explore the roles and mechanisms of the selected OTUs in ALI. Our screen identified OTUD1 in the OTU family as a deubiquitinase highly related to ALI. In the LPS-induced ALI model, deficiency of OTUD1 significantly ameliorated pulmonary edema, reduced permeability damage, and decreased lung immunocyte infiltration. Furthermore, RNA-seq analysis revealed that OTUD1 deficiency inhibited key pathways, including the IFN-γ/STAT1 and TNF-α/NF-κB axes, ultimately mitigating the severity of immune responses in ALI. In summary, our study highlights OTUD1 as a critical immunomodulatory factor in acute inflammation. These findings suggest that targeting OTUD1 could hold promise for the development of novel treatments against ALI/ARDS.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"649-661"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733986","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

Prenatal Inflammatory Exposure Predisposes Offspring to Chronic Kidney Diseases Via the Activation of the eIF2α-ATF4 Pathway. 产前炎症暴露通过激活 eIF2α-ATF4 通路使后代易患慢性肾病

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-06-24 DOI: 10.1007/s10753-024-02084-5

Jie Liu, Xin Chen, Jie Liu, Cuiping Peng, Fangjie Wang, Xiaoyong Huang, Shuhui Li, Ying Liu, Weinian Shou, Dayan Cao, Xiaohui Li

{"title":"Prenatal Inflammatory Exposure Predisposes Offspring to Chronic Kidney Diseases Via the Activation of the eIF2α-ATF4 Pathway.","authors":"Jie Liu, Xin Chen, Jie Liu, Cuiping Peng, Fangjie Wang, Xiaoyong Huang, Shuhui Li, Ying Liu, Weinian Shou, Dayan Cao, Xiaohui Li","doi":"10.1007/s10753-024-02084-5","DOIUrl":"10.1007/s10753-024-02084-5","url":null,"abstract":"It has recently become more recognized that renal diseases in adults can originate from adverse intrauterine (maternal) environmental exposures. Previously, we found that prenatal lipopolysaccharide (LPS) exposure can result in chronic renal inflammation, which leads to renal damage in older offspring rats. To test whether prenatal inflammatory exposure predisposes offspring to renal damage, a mouse model of oral adenine consumption-induced chronic kidney disease (CKD) was applied to offspring from prenatal LPS-treated mothers (offspring-pLPS) and age-matched control offspring of prenatal saline-treated mothers (offspring-pSaline). We found that offspring-pLPS mice presented with more severe renal collagen deposition and renal dysfunction after 4 weeks of adenine consumption than sex- and treatment-matched offspring-pSaline controls. To illustrate the underlying molecular mechanism, we subjected offspring-pLPS and offspring-pSaline kidneys to genome-wide transcriptomic analysis. Bioinformatic analysis of the sequencing data, together with further experimental confirmation, revealed a strong activation of the PERK-eIF2α-ATF4-mediated unfolded protein response (UPR) in offspring-pLPS kidneys, which likely contributed to the CKD predisposition seen in offspring-pLPS mice. More importantly, the specific eIF2α-ATF4 signaling inhibitor ISIRB was able to prevent adenine-induced CKD in the offspring-pLPS mice. Our findings suggest that the eIF2α-ATF4-mediated UPR, but not PERK, is likely the major disease-causing pathway in prenatal inflammatory exposure-induced CKD predisposition. Our study also suggests that targeting this signaling pathway is a potentially promising approach for CKD treatment.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"747-759"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442501","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

EZH2-H3K27me3-Mediated Epigenetic Silencing of DKK1 Induces Nucleus Pulposus Cell Pyroptosis in Intervertebral Disc Degeneration by Activating NLRP3 and NAIP/NLRC4. EZH2-H3K27me3介导的DKK1表观遗传沉默通过激活NLRP3和NAIP/NLRC4诱导椎间盘退行性变中的核髓细胞嗜热症。

IF 4.5 2区医学

Inflammation Pub Date : 2025-04-01 Epub Date: 2024-07-25 DOI: 10.1007/s10753-024-02096-1

Qijun Yao, Yue Lei, Yongxu Zhang, Haoran Chen, Xiaowei Dong, Zhiqiang Ye, Haidong Liang

{"title":"EZH2-H3K27me3-Mediated Epigenetic Silencing of DKK1 Induces Nucleus Pulposus Cell Pyroptosis in Intervertebral Disc Degeneration by Activating NLRP3 and NAIP/NLRC4.","authors":"Qijun Yao, Yue Lei, Yongxu Zhang, Haoran Chen, Xiaowei Dong, Zhiqiang Ye, Haidong Liang","doi":"10.1007/s10753-024-02096-1","DOIUrl":"10.1007/s10753-024-02096-1","url":null,"abstract":"Nucleus pulposus (NP) cell pyroptosis is crucial for intervertebral disc degeneration (IDD). However, the precise mechanisms underlying pyroptosis in IDD remain elusive. Therefore, this study aimed to investigate how dickkopf-1 (DKK1) influences NP cell pyroptosis and delineate the regulatory mechanisms of IDD. Behavioral tests and histological examinations were conducted in rat IDD models to assess the effect of DKK1 on the structure and function of intervertebral discs. Detected pyroptosis levels using Hoechst 33,342/propidium iodide (PI) double staining, and determined pyroptosis-related protein expression via western blotting. The cellular mechanisms of DKK1 in pyroptosis were explored in interleukin (IL)-1β-induced NP cells transfected with or without DKK1 overexpression plasmids (oe-DKK1). In addition, IL-1β-treated NP cells transfected with sh-EZH2 and/or sh-DKK1 were utilized to clarify the interplay between the enhancer of zeste homologue 2 (EZH2) and DKK1 in pyroptosis. Additionally, the epigenetic regulation of DKK1 by EZH2 was explored in NP cells treated with the EZH2 inhibitors GSK126/DZNep. DKK1 expression decreased in IDD rats. Transfection with oe-DKK1 reduced pro-inflammatory factors and extracellular matrix markers in IDD rats. In IL-1β-induced NP cells, DKK1 overexpression suppressed pyroptosis and inhibited the NLRP3 and NAIP/NLRC4 inflammasome activation. EZH2 knockdown increased DKK1 expression and reduced pyroptosis-related proteins. Conversely, DKK1 downregulation reversed the inhibitory effects of EZH2 knockdown on pyroptosis. Furthermore, EZH2 suppressed DKK1 expression via H3K27 methylation at the DKK1 promoter. EZH2 negatively regulates DKK1 expression via H3K27me3 methylation, promoting NP cell pyroptosis in IDD patients. This regulatory effect involves the activation of NLRP3 and NAIP/NLRC4 inflammasomes.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"902-918"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758483","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