International immunopharmacology最新文献_第6页

MMP-9 and TIMPs profiles in sulfur mustard-exposed individuals with serious lung complications.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-10 DOI: 10.1016/j.intimp.2024.113777

Faramarz Fallahi, Nayere Askari, Tahereh Jamali, Sara Parsapour, Hassan Ghasemi, Jalaledin Shams, Roya Yaraee, Zeinab Ghazanfari, Tooba Ghazanfari

{"title":"MMP-9 and TIMPs profiles in sulfur mustard-exposed individuals with serious lung complications.","authors":"Faramarz Fallahi, Nayere Askari, Tahereh Jamali, Sara Parsapour, Hassan Ghasemi, Jalaledin Shams, Roya Yaraee, Zeinab Ghazanfari, Tooba Ghazanfari","doi":"10.1016/j.intimp.2024.113777","DOIUrl":"10.1016/j.intimp.2024.113777","url":null,"abstract":"Sulfur mustard (SM), a chemical weapon used in the Iraq-Iran war, can pose severe health risks, especially to the lungs. Dysregulation of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) have been implicated in various inflammatory lung diseases. This study compares the levels of MMPs and TIMPs in the serum and sputum of veterans with serious lung complications to a control group. Serum and sputum samples were collected and analyzed using the ELISA sandwich method. Differences between SM-exposed and control groups were assessed statistically. The serum levels of TIMP-4 and MMP-9/TIMP-4 were significantly lower and higher in the SM-exposed group respectively compared to the control group. In SM-exposed individuals resembling Bronchiolitis Obliterans (BO), Chronic Bronchitis (CB), and Asthma, TIMP-4 levels were lower than controls, while TIMP-2 levels were higher in those with CB. Although the increased TIMP-2 levels in these patients align with COPD studies, differences were observed in other factors with COPD and asthma-related MMP-9 and TIMP-4 findings. Assessment of serum levels of these factors based on severity reveals lower MMP-9/TIMP-4 levels in the severe group compared to the mild-moderate group. Individuals exposed to SM exhibit distinct MMP and TIMP profiles, with significantly lower TIMP-4 levels and higher MMP-9/TIMP-4 ratios, compared to controls. These profiles vary across different lung conditions, indicating a unique disease mechanism in SM-exposed individuals. This distinctive profile supports the classification of this condition as 'Mustard Lung.' Further research is needed to elucidate these mechanisms for targeted therapeutic interventions.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113777"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806953","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

Ginsenoside reprogramming microglia through the FGF/FGFR1 inhibits post traumatic stress disorder.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-12 DOI: 10.1016/j.intimp.2024.113763

Huangao Zhou, Hao Pan, Xiangwei Li, Lan Huang, Ruiqi Zhang, Xianliang Yan, Jianing Xu

{"title":"Ginsenoside reprogramming microglia through the FGF/FGFR1 inhibits post traumatic stress disorder.","authors":"Huangao Zhou, Hao Pan, Xiangwei Li, Lan Huang, Ruiqi Zhang, Xianliang Yan, Jianing Xu","doi":"10.1016/j.intimp.2024.113763","DOIUrl":"10.1016/j.intimp.2024.113763","url":null,"abstract":"Post traumatic stress disorder (PTSD) is a serious and persistent mental diseases. Nowadays, Treatment of PTSD patients in clinical practice is mainly based on drug therapy accompanied by psychological therapy. However, the therapeutic effect is unsatisfactory. It is urgent to detect how to treat PTSD patients. Here, we found that ginsenoside can significantly relieve PTSD symptoms in mice model. Rg3, one of the main pharmacological components of ginsenoside, prevents PTSD by promoting alternatively activated M2 phenotype microglia while inhibiting classically activated inflammatory M1 phenotype microglia. Mechanistically, Rg3 up-regulates fibroblast growth factor receptor 1 (FGFR1) expression in microglia to suppress excessive activation of microglia and reduce neuronal apoptosis. Importantly, knocking down FGFR1 expression in BV2 cells promoted a pro-inflammatory phenotype of BV2 cells, while over-expressing FGFR1 reversed this effect. In vivo PTSD mice model results showed that knockdown FGFR1 prevents the therapeutic effect of Rg3, which indicates that FGFR1 is an essential target of PTSD. Our results reveal that Rg3 may be a potential drug to treat PTSD patients.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113763"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822151","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 "S100A4 reprofiles lipid metabolism in mast cells via RAGE and PPAR-γ signaling pathway" [Int Immunopharmacol. 128 (2024) 111555].

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-07 DOI: 10.1016/j.intimp.2024.113741

Mo Shihui, Yan Shirong, Li Jing, He Jingjing, Wu Tongqian, Tao Tian, Wang Chenyu, Yu Fang

引用次数: 0

Neuro-immune regulation in allergic Diseases: Role of neuropeptides. 过敏性疾病中的神经免疫调节：神经肽的作用

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-11 DOI: 10.1016/j.intimp.2024.113771

Cuiying He, Qian Wang, Jinyan Gao, Hongbing Chen, Ping Tong

{"title":"Neuro-immune regulation in allergic Diseases: Role of neuropeptides.","authors":"Cuiying He, Qian Wang, Jinyan Gao, Hongbing Chen, Ping Tong","doi":"10.1016/j.intimp.2024.113771","DOIUrl":"10.1016/j.intimp.2024.113771","url":null,"abstract":"The role of neuro-immune interaction in allergic diseases, a group of common immune system diseases, has garnered increasing attention. Neuropeptides, as a crucial component of neuro-immune crosstalk with local neuroendocrine and signaling functions, play a significant role that must not be overlooked. Neuropeptides are released by neurons and even some immune cells, and mediate neuro-immune crosstalk by activating relevant specific receptors on immune cells. Recent studies have found that neuropeptides have a certain regulatory effect on allergic diseases, which could be beneficial or detrimental for the development of allergic diseases. Nevertheless, the precise mechanism of neuropeptides in allergic diseases remains unclear, particularly in the context of food allergy where their role is poorly understood. This review summarized the interplay between neuropeptides and different immune cells, as well as their current research progress in several common allergic diseases: atopic dermatitis, allergic asthma, and food allergy. It is evident that neuropeptides such as substance P, calcitonin gene-related peptide, vasoactive intestinal peptide, and neuromedin U, exert important regulatory effects on allergic diseases, yet further investigation is required to fully elucidate their mechanisms of action, which may contribute to better understanding of the onset and progression of allergic diseases and finding better immunomodulatory strategies.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113771"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817906","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

Ubiquitin-like modifier-activating enzyme 1 as a potential therapeutic target for aortic dissection.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-04 DOI: 10.1016/j.intimp.2024.113742

Yao Wang, Jinjin Zhang, Yunsong Wang, Feng Wu, Baoshen Song, Jiatian Li, Qiuyue Lin, Yunpeng Xie, Yunlong Xia, Xiangbo An, Jiawei Liao

{"title":"Ubiquitin-like modifier-activating enzyme 1 as a potential therapeutic target for aortic dissection.","authors":"Yao Wang, Jinjin Zhang, Yunsong Wang, Feng Wu, Baoshen Song, Jiatian Li, Qiuyue Lin, Yunpeng Xie, Yunlong Xia, Xiangbo An, Jiawei Liao","doi":"10.1016/j.intimp.2024.113742","DOIUrl":"10.1016/j.intimp.2024.113742","url":null,"abstract":"Aortic dissection (AD) is a life-threatening aortopathy with no specific pharmacological therapy. Ubiquitination, a highly orchestrated enzymatic cascade involving sequential E1-E2-E3 interactions, is suggested to contribute to the disease pathogenesis. However, the specific role of E1 enzymes in AD progression remains unknown. In this study, we analyzed the aortic transcriptional profiles of a human ascending dissection dataset (GSE52093) and identified ubiquitin-like modifier-activating enzyme 1 (UBA1) as a significantly up-regulated E1 enzyme in human AD. This finding was further corroborated by immunohistochemistry and RT-qPCR in a mouse model of AD induced by β-aminopropionitrile (BAPN). Treatment of TAK-243, a specific UBA1 inhibitor, prevented BAPN-induced AD formation in mice and attenuated aortic medial degeneration, as evidenced by decreased elastin fragmentation (evaluated by EVG scoring), reduced vascular smooth muscle cell loss (visualized by α-SMA immunohistochemistry), and less extracellular matrix degradation (indicated by diminished MMP2 and MMP9 expression in immunohistochemistry and RT-qPCR). Furthermore, TAK-243 treatment attenuated lesional macrophage accumulation and activation, as demonstrated by CD68 immunohistochemistry and RT-qPCR analysis of aortic pro-inflammatory cytokine expression. In vitro, UBA1 activation was observed in macrophages (RAW264.7 cells) treated with angiotensin II (AngII), and TAK-243 significantly reduced AngII-induced macrophage activation, at least partially through the inhibition of IκBα and NF-κB p65 phosphorylation. In conclusion, we demonstrate that UBA1 may facilitate AD progression by promoting macrophage activation via the NF-κB signaling pathway. These findings reveal a pathogenic role for the E1 enzyme UBA1 in AD and show a pharmacological potential of UBA1-targeted therapy against this disease.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113742"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785639","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

Downregulation of HSPA12A protects heart against sepsis through suppressing mTOR-mediated inflammatory response in cardiomyocytes.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-05 DOI: 10.1016/j.intimp.2024.113721

Yunfan Li, Xiaojin Zhang, Guohua Jiang, Xinxu Min, Qiuyue Kong, Li Liu, Jun Wu, Zhengnian Ding

{"title":"Downregulation of HSPA12A protects heart against sepsis through suppressing mTOR-mediated inflammatory response in cardiomyocytes.","authors":"Yunfan Li, Xiaojin Zhang, Guohua Jiang, Xinxu Min, Qiuyue Kong, Li Liu, Jun Wu, Zhengnian Ding","doi":"10.1016/j.intimp.2024.113721","DOIUrl":"10.1016/j.intimp.2024.113721","url":null,"abstract":"Objective: Over-activated immune response in hearts is the main pathological feature of septic cardiomyopathy, a fatal complication of sepsis with high mortality. Autophagy is capable to limit immune response by removing inflammatory mediators. Heat shock protein A12A (HSPA12A) encodes an atypical member of HSP70 family. This study aimed to investigate the role of HSPA12A in septic cardiomyopathy.Methods: Sepsis was induced by cecal ligation and puncture (CLP) for 6 h in mice in vivo or by LPS treatment for 24 h in primary cardiomyocytes in vitro. HSPA12A knockout (Hspa12a-/-) mice were generated by cre-loxp system. Echocardiography was performed to assess cardiac function. TUNEL and propidium iodide (PI) staining was used to indicate cardiomyocyte death. Inflammation-related factors were examined by qPCR and immunoblotting. Autophagy was evaluated by levels of LC3-II and p62.Results: Sepsis decreased HSPA12A expression in hearts and cardiomyocytes, while HSPA12A knockout in mice attenuated sepsis-induced cardiomyocyte death and cardiac dysfunction. Sepsis-induced activation of TLR4/MyD88/NF-κB-mediated inflammation was inhibited in hearts by HSPA12A knockout whereas was enhanced by HSPA12A overexpression in cardiomyocytes. Moreover, HSPA12A overexpression activated mTOR and inhibited autophagy in cardiomyocytes, while inhibition of mTOR by rapamycin diminished the HSPA12A-induced autophagy inhibition, inflammation activation, and cardiomyocyte death in septic cardiomyocytes.Conclusion: Downregulation of HSPA12A inhibited mTOR to activated autophagy, thereby suppressed inflammatory response, and ultimately attenuated septic cardiomyopathy. Our findings identified HSPA12A as a driver for septic cardiomyopathy development, and strategies that inhibit HSPA12A in cardiomyocytes might be a potential therapeutic intervention.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113721"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791797","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

Neutrophils promote laser-induced choroidal neovascularization by increasing pro-inflammatory cytokines secretion and cell cycle arrest in retinal pigment epithelium.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-06 DOI: 10.1016/j.intimp.2024.113735

Qian Fan, Xian Song, Mengyao Li, Qian Xu, Chenfei Yan, Haiming Li, Yi Qu

{"title":"Neutrophils promote laser-induced choroidal neovascularization by increasing pro-inflammatory cytokines secretion and cell cycle arrest in retinal pigment epithelium.","authors":"Qian Fan, Xian Song, Mengyao Li, Qian Xu, Chenfei Yan, Haiming Li, Yi Qu","doi":"10.1016/j.intimp.2024.113735","DOIUrl":"10.1016/j.intimp.2024.113735","url":null,"abstract":"Inflammation is hypothesized to have essential functions in the development of wet age-related macular degeneration (AMD). Polymorphonuclear neutrophils (PMNs), recognized as major players in inflammation, are typically the first leukocytes to be recruited to an inflammatory site. Previous studies have identified neutrophil aggregates in the lesion site of the choroidal neovascularization model, and systemic depletion of neutrophils in adult mice is associated with reduced choroidal neovascularization (CNV) area, suggesting a pivotal role of PMNs in CNV pathogenesis. Here, we investigate the role of neutrophils in promoting CNV, a key feature of wet AMD. The malfunction and demise of retinal pigment epithelium cells are essential elements in CNV pathogenesis. Our hypothesis posits that neutrophils exacerbate CNV by influencing pro-inflammatory cytokines secreted by retinal pigment epithelium (RPE) cells. Using in vivo laser-induced CNV models with mice and in vitro experiments with the human ARPE-19 cell line, we demonstrated that co-culturing neutrophils with ARPE-19 cells induces an increase in pro-inflammatory cytokines and leads to S-phase cell cycle arrest, potentially through the induction of double-strand breaks (DSBs). Further exploration of this interaction revealed a potential pathway involving reactive oxygen species (ROS) and microRNA-23a, wherein PMNs induce DSBs by initiating the downregulation of LB1 via microRNA-23a. Additionally, we found that dHL-60 cell line could serve as a substitute for primary PMNs, highlighting its potential as a valuable tool in experimental models involving interactions with retinal cells. Our findings underscore the significant role of neutrophils in CNV pathogenesis, providing insights into potential therapeutic targets for wet AMD.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113735"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791916","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

Integrating network pharmacology and animal experimental validation to investigate the mechanism of lotus leaf in obesity.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-08 DOI: 10.1016/j.intimp.2024.113719

Haojing Li, Wenli Li, Yuanyuan Wu, Huimin Wu, Xiaojun Cai

{"title":"Integrating network pharmacology and animal experimental validation to investigate the mechanism of lotus leaf in obesity.","authors":"Haojing Li, Wenli Li, Yuanyuan Wu, Huimin Wu, Xiaojun Cai","doi":"10.1016/j.intimp.2024.113719","DOIUrl":"10.1016/j.intimp.2024.113719","url":null,"abstract":"Background: Lotus leaf and its extracts have been reported to exert various beneficial effects; however, their anti-obesity mechanisms remain relatively unclear. Therefore, we investigated the mechanism by which lotus leaf regulates obesity using network pharmacology, molecular docking, and animal experimentation.Methods: Network pharmacology was used to identify potential targets and pathways through which lotus leaf regulates obesity. Molecular docking technology was used to verify the interaction between lotus leaves and core targets of obesity. Additionally, a rat model of obesity induced using a high-fat diet was established to examine the anti-obesity effects of lotus leaf. Moreover, western blotting was performed to examine the expression levels of the target proteins and elucidate the molecular mechanisms of lotus leaf.Results: Quercetin, nuciferin, catechin, kaempferol, and isorhamnetin were identified as the main active compounds in the lotus leaves involved in obesity treatment. Network pharmacology analysis identified fibroblast growth factor (FGF) 15 and farnesoid X receptor (FXR) as core targets of lotus leaf, and the AGE-RAGE signaling pathway in diabetic complications, neuroactive ligand-receptor interactions, insulin resistance, and cancer pathways, as biomechanistic pathways by which lotus leaf ameliorates obesity. Additionally, molecular docking analysis indicated a strong binding affinity between the main active ingredients of lotus leaf and the core targets. Moreover, western blotting showed that lotus leaf significantly downregulated FGF15 and FXR protein expression in intestinal tissues.Conclusions: Lotus leaf ameliorates obesity through several pathways, including by downregulating FGF15 and FXR, providing a novel basis for the development of natural drug therapy for obesity.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113719"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794669","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

Neutrophil extracellular traps promote the activation of the NLRP3 inflammasome and PBMCs pyroptosis via the ROS-dependent signaling pathway in Kawasaki disease.

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-07 DOI: 10.1016/j.intimp.2024.113783

Jing Jin, Yan Zhao, Yuying Fang, Yuting Pan, Panpan Wang, Zhidan Fan, Haiguo Yu

{"title":"Neutrophil extracellular traps promote the activation of the NLRP3 inflammasome and PBMCs pyroptosis via the ROS-dependent signaling pathway in Kawasaki disease.","authors":"Jing Jin, Yan Zhao, Yuying Fang, Yuting Pan, Panpan Wang, Zhidan Fan, Haiguo Yu","doi":"10.1016/j.intimp.2024.113783","DOIUrl":"10.1016/j.intimp.2024.113783","url":null,"abstract":"Kawasaki disease (KD) is an acute systemic vasculitis predominantly affecting infants and children under the age of 5. Recent studies have indicated that excessively released neutrophil extracellular traps (NETs) are involved in the progression of vasculitis. The purpose of this study was to investigate the role of NETs, especially their interaction with peripheral blood mononuclear cells (PBMCs), in the pathogenesis of KD. First, we demonstrated that the levels of NETs (cfDNA, MPO, and NE) in the serum of KD patients were significantly higher than those in healthy controls (HCs) and notably decreased after treatment. During the acute phase of KD, inflammatory markers (CRP and ESR) were positively correlated with NETs levels. Furthermore, we observed that neutrophils from KD patients in the acute phase produced elevated levels of NETs, and aspirin could effectively regulate the release of NETs. Additionally, NETs significantly increased the mRNA levels of NLRP3 and IL-1β in PBMCs, as well as the protein expression of NLRP3, caspase-1, ASC and gasdermin D, and the concentration of IL-1β in the cell supernatant. Moreover, NETs stimulated the production of reactive oxygen species (ROS) in PBMCs. N-acetylcysteine significantly reduced the expression of inflammatory factors and pyroptosis-related proteins in PBMCs. In conclusion, our findings suggest that NETs induce the generation of ROS, which in turn activates the NLRP3 inflammasome to mediate PBMCs pyroptosis and perpetuate inflammation in KD patients. This study reveals that targeting NETs or ROS could be a potential therapeutic approach for alleviating systemic inflammation, and that NETs may be a novel target for aspirin in the treatment of KD patients.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113783"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794672","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

Unlocking the therapeutic potential of WISP-1: A comprehensive exploration of its role in age-related musculoskeletal disorders. 挖掘 WISP-1 的治疗潜力：全面探索其在与年龄相关的肌肉骨骼疾病中的作用。

IF 4.8 2区医学

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-11 DOI: 10.1016/j.intimp.2024.113791

Wenhao Lu, Wenjie Feng, Haozu Zhen, Shide Jiang, Yusheng Li, Shuguang Liu, Qin Ru, Wenfeng Xiao

{"title":"Unlocking the therapeutic potential of WISP-1: A comprehensive exploration of its role in age-related musculoskeletal disorders.","authors":"Wenhao Lu, Wenjie Feng, Haozu Zhen, Shide Jiang, Yusheng Li, Shuguang Liu, Qin Ru, Wenfeng Xiao","doi":"10.1016/j.intimp.2024.113791","DOIUrl":"10.1016/j.intimp.2024.113791","url":null,"abstract":"As the global population ages, the incidence of age-related musculoskeletal diseases continues to increase, driven by numerous complex and poorly understood factors. WNT-1 inducible secreted protein 1 (WISP-1), a secreted matrix protein, plays a critical role in the growth and development of the musculoskeletal system, including chondrogenesis, osteogenesis, and myogenesis. Numerous in vivo and in vitro studies have demonstrated that WISP-1 is significantly upregulated in age-related musculoskeletal conditions, such as osteoarthritis, osteoporosis, and sarcopenia, suggesting its involvement in the pathogenesis of these diseases. Regulating WISP-1 expression holds promise as a therapeutic strategy for improving musculoskeletal function, potentially offering new avenues for treating age-related musculoskeletal diseases in clinical practice. This review highlights the signaling pathways associated with WISP-1, its physiological roles within the musculoskeletal system, and its therapeutic potential in treating age-related musculoskeletal disorders.","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113791"},"PeriodicalIF":4.8,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817992","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