Inflammation and regeneration最新文献

{"title":"CD147-high classical monocytes: a cellular biomarker for COVID-19 disease severity and treatment response.","authors":"Teruaki Murakami, Yuta Yamaguchi, Saori Amiya, Yuko Yoshimine, Shinichiro Nameki, Yasutaka Okita, Yasuhiro Kato, Haruhiko Hirata, Yoshito Takeda, Atsushi Kumanogoh, Takayoshi Morita","doi":"10.1186/s41232-025-00371-8","DOIUrl":"10.1186/s41232-025-00371-8","url":null,"abstract":"<p><strong>Background: </strong>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to severe coronavirus disease 2019 (COVID-19), which is characterized by cytokine storm and organ dysfunction. The spike S1 subunit induces inflammatory cytokine production, but the immune cell subsets that respond to S1 stimulation and contribute to disease severity remain unclear.</p><p><strong>Methods: </strong>We analyzed serum samples and peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 (moderate: n = 7; severe: n = 25) and healthy controls (n = 38). Using mass cytometry (cytometry by time-of-flight; CyTOF), we analyzed immune cell responses to S1 subunit stimulation in PBMCs from healthy donors and patients with COVID-19. We examined correlations among identified cell populations, serum cytokine levels, and clinical parameters.</p><p><strong>Results: </strong>Serum S1 subunit levels correlated with disease severity and inflammatory cytokine concentrations. S1 subunit stimulation induced dose-dependent cytokine production from PBMCs, predominantly from myeloid cells. CyTOF analysis identified classical monocytes with high CD147 expression (CD147hi cMono) as the primary source of S1-induced cytokines. The proportion of CD147hi cMono increased significantly in severe COVID-19 and decreased with clinical improvement. The frequency of CD147hi cMono showed a stronger positive correlation with clinical severity markers in younger patients compared to older patients.</p><p><strong>Conclusions: </strong>CD147hi cMono are the primary cellular source of S1-induced inflammatory cytokines and may serve as potential biomarkers for monitoring COVID-19 severity and treatment response.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural repair mechanisms after ischemic stroke.","authors":"Koshi Irisa, Takashi Shichita","doi":"10.1186/s41232-025-00372-7","DOIUrl":"10.1186/s41232-025-00372-7","url":null,"abstract":"<p><p>Ischemic stroke triggers inflammation that promotes neuronal injury, leading to disruption of neural circuits and exacerbated neurological deficits in patients. Immune cells contribute to not only the acute inflammatory responses but also the chronic neural repair. During the post-stroke recovery, reparative immune cells support the neural circuit reorganization that occurs around the infarct region to connect broad brain areas. This review highlights the time-dependent changes of neuro-immune interactions and reorganization of neural circuits after ischemic brain injury. Understanding the molecular mechanisms involving immune cells in acute inflammation, subsequent neural repair, and neuronal circuit reorganization that compensate for the lost brain function is indispensable to establish treatment strategies for stroke patients.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial transcriptomics in autoimmune rheumatic disease: potential clinical applications and perspectives.","authors":"Atsuko Tsujii Miyamoto, Hiroshi Shimagami, Atsushi Kumanogoh, Masayuki Nishide","doi":"10.1186/s41232-025-00369-2","DOIUrl":"10.1186/s41232-025-00369-2","url":null,"abstract":"<p><p>Spatial transcriptomics is a cutting-edge technology that analyzes gene expression at the cellular level within tissues while integrating spatial location information. This concept, which combines high-plex RNA sequencing with spatial data, emerged in the early 2010s. Spatial transcriptomics has rapidly expanded with the development of technologies such as in situ hybridization, in situ sequencing, in situ spatial barcoding, and microdissection-based methods. Each technique offers advanced mapping resolution and precise spatial assessments at the single-cell level. Over the past decade, the use of spatial transcriptomics on clinical samples has enabled researchers to identify gene expressions in specific diseased foci, significantly enhancing our understanding of cellular interactions and disease processes. In the field of rheumatology, the complex and elusive pathophysiology of diseases such as rheumatoid arthritis, systemic lupus erythematosus, and Sjögren's syndrome remains a challenge for personalized treatment. Spatial transcriptomics provides insights into how different cell populations interact within disease foci, such as the synovial tissue, kidneys, and salivary glands. This review summarizes the development of spatial transcriptomics and current insights into the pathophysiology of autoimmune rheumatic diseases, focusing on immune cell distribution and cellular interactions within tissues. We also explore the potential of spatial transcriptomics from a clinical perspective and discuss the possibilities for translating this technology to the bedside.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inactivation of the CMAH gene and deficiency of Neu5Gc play a role in human brain evolution.","authors":"Yuxin Liu, Jinhong Li, Qicai Liu","doi":"10.1186/s41232-025-00368-3","DOIUrl":"10.1186/s41232-025-00368-3","url":null,"abstract":"<p><p>During human evolution, some genes were lost or silenced from the genome of hominins. These missing genes might be the key to the evolution of humans' unique cognitive skills. An inactivation mutation in CMP-N-acetylneuraminic acid hydroxylase (CMAH) was the result of natural selection. The inactivation of CMAH protected our ancestors from some pathogens and reduced the level of N-glycolylneuraminic acid (Neu5Gc) in brain tissue. Interestingly, the low level of Neu5Gc promoted the development of brain tissue, which may have played a role in human evolution. As a xenoantigen, Neu5Gc may have been involved in brain evolution by affecting neural conduction, neuronal development, and aging.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CX3CR1⁺ age-associated CD4⁺ T cells contribute to synovial inflammation in late-onset rheumatoid arthritis.","authors":"Mitsuhiro Akiyama, Sohma Wakasugi, Keiko Yoshimoto, Koichi Saito, Sho Ishigaki, Risa Inukai, Yoshiyuki Matsuno, Waleed Alshehri, Yasushi Kondo, Yuko Kaneko","doi":"10.1186/s41232-025-00367-4","DOIUrl":"10.1186/s41232-025-00367-4","url":null,"abstract":"<p><strong>Background: </strong>Recent evidence suggests that clonally expanded cytotoxic T cells play a role in various autoimmune diseases. Late-onset rheumatoid arthritis (LORA) exhibits unique characteristics compared to other RA forms, suggesting distinct immunological mechanisms. This study aimed to examine the involvement of cytotoxic T cells in LORA.</p><p><strong>Methods: </strong>Fresh peripheral blood samples were collected from 78 treatment-naïve active RA patients, 12 with difficult-to-treat RA, and 16 healthy controls. Flow cytometry was employed to measure the proportions of CX3CR1⁺cytotoxic CD4⁺ and CD8⁺ T cells in these samples. Additionally, immunohistochemical staining was performed on lymphoid node and synovial biopsy samples from patients with RA.</p><p><strong>Results: </strong>CX3CR1⁺cytotoxic CD4⁺ T cells were specifically increased in untreated, active patients with LORA, displaying features of CXCR3^mid age-associated T helper cells known as \"ThA\". CX3CR1⁺CD4⁺ T cells were identified as a cytotoxic ThA subset, as nearly all of these cells specifically expressed granzyme B. These cells were observed in enlarged lymph nodes and were found to infiltrate synovial tissues from patients with LORA. The proportions of CX3CR1⁺CD4⁺ T cells positively correlated with arthritis activity in LORA. The number of cells decreased after treatment with methotrexate, tumor necrosis factor inhibitors, and interleukin-6 inhibitors, whereas T-cell activation modulators did not affect them. Moreover, PD-1⁺CD38⁺CX3CR1⁺CD4⁺ T cells were identified as a treatment-resistant T cell subset that was characteristically increased in difficult-to-treat RA. CX3CR1⁺CD8⁺ T cells showed no significant difference between RA patients and healthy individuals, and no correlation with disease activity was observed. However, a correlation with age was observed in RA patients.</p><p><strong>Conclusions: </strong>Our findings suggest that the immunopathogenesis of RA differs by age of onset, with CX3CR1⁺ age-associated cytotoxic CD4⁺ T cells playing a significant role in LORA. Additionally, the presence of a specific CX3CR1⁺ T cell subset may be linked to treatment resistance.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-organ frailty is enhanced by periodontitis-induced inflammaging.","authors":"Yoshitaka Kase, Satoru Morikawa, Yuji Okano, Tatsuya Hosoi, Takazumi Yasui, Yoko Taki-Miyashita, Mitsutaka Yakabe, Maraku Goto, Kazuyuki Ishihara, Sumito Ogawa, Taneaki Nakagawa, Hideyuki Okano","doi":"10.1186/s41232-025-00366-5","DOIUrl":"10.1186/s41232-025-00366-5","url":null,"abstract":"<p><strong>Background: </strong>The incidence of periodontitis is high in older individuals. However, its impact on multi-organ frailty remains unclear. We developed mouse models with varying severity and duration of periodontitis to examine its effects.</p><p><strong>Methods: </strong>We generated mouse models with mild and severe periodontitis, categorizing the disease duration into 3-month and 5-month periods for analysis. The organs assessed for frailty included the gastrocnemius muscle, soleus muscle, brain, and femur.</p><p><strong>Results: </strong>Our study found that periodontitis induced systemic inflammation resembling inflammaging and other symptoms characteristic of age-induced frailty. Notably, muscle impairment developed specifically in slow-twitch muscles, and the femur emerged as the most vulnerable bone, exhibiting reduced bone mineral density even with mild and short-duration periodontitis. This condition resulted in the co-occurrence of bone fragility and slow-twitch muscle dysfunction. Cognitive function assessment revealed increased activated microglia and decreased adult neurogenesis in the hippocampus, impairing spatial learning. Thus, periodontitis induced both physical and cognitive frailties. Therapeutic intervention for the periodontitis, which halted the exacerbation of bone resorption markers, did not restore femur bone mineral density.</p><p><strong>Conclusion: </strong>This study underscores the role of periodontitis in inducing multifaceted organ frailty with vulnerability, varying by organ, and the necessity of early intervention, particularly regarding bone density loss.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11789345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143082420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amelioration of liver fibrosis with autologous macrophages induced by IL-34-based condition.","authors":"Yuichi Igarashi, Haruka Wada, Masato Muto, Ryohei Sone, Yoshinori Hasegawa, Ken-Ichiro Seino","doi":"10.1186/s41232-025-00364-7","DOIUrl":"10.1186/s41232-025-00364-7","url":null,"abstract":"<p><strong>Background: </strong>For the treatment of liver fibrosis, several novel cell therapies have been proposed. Autologous macrophage therapy has been reported as one of the promising treatments. So far, most studies have used colony-stimulating factor 1 (CSF-1) to induce the differentiation of macrophage progenitor cells. The receptor for CSF-1, CSF-1R possesses another ligand, interleukin 34. However, the therapeutic capacity for liver fibrosis by interleukin 34-induced macrophages has not been evaluated.</p><p><strong>Methods: </strong>We have employed acute (bile duct ligation) and chronic (administration of carbon tetrachloride or thioacetamide) liver fibrosis models. Using these models, we evaluated the therapeutic capacity of macrophages induced by interleukin 34-based conditions. In most experiments, interleukin 4 was also added to the differentiation process to induce alternative-activated macrophages. As a mechanism analysis, we have examined liver inflammation and damage, the status of stellate cells, and the immunosuppressive capacity of the macrophages. Human macrophages were differentiated from CD14⁺ monocytes and analyzed.</p><p><strong>Results: </strong>In both acute and chronic liver damage experiments, interleukin 34-induced macrophages significantly ameliorated liver fibrosis. The addition of interleukin 4 to the differentiation process resulted in an increase of obtained macrophages and a bias to alternative activated macrophages (so-called M2). The alternative activated macrophages (M2-type) showed a reproducible therapeutic effect of liver fibrosis with a suppression of parameters of liver inflammation and damage, stellate cells, and T cell activation. Similar macrophages could be differentiated from human CD14⁺ monocytes in the presence of interleukin 34 plus interleukin 4, and a therapeutic effect was observed using a humanized mouse model.</p><p><strong>Conclusions: </strong>Interleukin 34-induced macrophages, particularly when additionally stimulated with interleukin 4, significantly ameliorated the liver fibrosis.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human PBMC-based humanized mice exhibit myositis features and serve as a drug evaluation model.","authors":"Akiko Nishidate, Kana Takemoto, Yuki Imura, Mikako Murase, Ryu Yamanaka, Manami Kikuchi, Junpei Anan, Sayuka Kato, Airi Akatsuka, Sachiko Mochizuki, Yuzo Koda","doi":"10.1186/s41232-025-00365-6","DOIUrl":"10.1186/s41232-025-00365-6","url":null,"abstract":"<p><p>Idiopathic inflammatory myopathies (IIMs) are a group of autoimmune disorders characterized by immune cell infiltration of muscle tissue accompanied by inflammation. Treatment of IIMs is challenging, with few effective therapeutic options due to the lack of appropriate models that successfully recapitulate the features of IIMs observed in humans. In the present study, we demonstrate that immunodeficient mice transplanted with human peripheral blood mononuclear cells (hPBMCs) exhibit the key pathologic features of myositis observed in humans and develop graft-versus-host disease. The hPBMC mice exhibit elevated serum levels of creatine kinase and aspartate transaminase, markers of myositis, and increased expression levels of myositis-related genes, such as vascular cell adhesion molecule 1, intercellular adhesion molecule 1, and serum amyloid A1, in muscle tissues. Histopathologic and flow cytometric analyses reveal the infiltration of CD8⁺ T cells in the muscle tissue of hPBMC mice, similar to that observed in patients with myositis, particularly in those with polymyositis. Transplantation of CD8⁺ T cell-depleted hPBMC leads to a significant reduction in polymyositis-like symptoms, in agreement with previous studies demonstrating CD8⁺ T cells as the main pathologic drivers of polymyositis. Furthermore, the transcriptome analysis of muscle tissue from hPBMC mice reveal extensive upregulation of characteristic genes of polymyositis, providing further support that hPBMC mice accurately reflect the pathophysiology of myositis in humans. Finally, administration of prednisolone or tacrolimus, which are commonly used for IIM treatment, leads to significant alleviation of myositis findings. Therefore, we propose that hPBMC mice should be considered as a model that accurately reflects the pathophysiology of myositis in human patients.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ca²⁺ signaling in vascular smooth muscle and endothelial cells in blood vessel remodeling: a review.","authors":"Yoshiaki Suzuki, Wayne R Giles, Gerald W Zamponi, Rubii Kondo, Yuji Imaizumi, Hisao Yamamura","doi":"10.1186/s41232-024-00363-0","DOIUrl":"10.1186/s41232-024-00363-0","url":null,"abstract":"<p><p>Vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) act together to regulate blood pressure and systemic blood flow by appropriately adjusting blood vessel diameter in response to biochemical or biomechanical stimuli. Ion channels that are expressed in these cells regulate membrane potential and cytosolic Ca²⁺ concentration ([Ca²⁺]_cyt) in response to such stimuli. The subsets of these ion channels involved in Ca²⁺ signaling often form molecular complexes with intracellular molecules via scaffolding proteins. This allows Ca²⁺ signaling to be tightly controlled in localized areas within the cell, resulting in a balanced vascular tone. When hypertensive stimuli are applied to blood vessels for extended periods, gene expression in these vascular cells can change dramatically. For example, alteration in ion channel expression often induces electrical remodeling that produces a depolarization of the membrane potential and elevated [Ca²⁺]_cyt. Coupled with endothelial dysfunction blood vessels undergo functional remodeling characterized by enhanced vasoconstriction. In addition, pathological challenges to vascular cells can induce inflammatory gene products that may promote leukocyte infiltration, in part through Ca²⁺-dependent pathways. Macrophages accumulating in the vascular adventitia promote fibrosis through extracellular matrix turnover, and cause structural remodeling of blood vessels. This functional and structural remodeling often leads to chronic hypertension affecting not only blood vessels, but also multiple organs including the brain, kidneys, and heart, thus increasing the risk of severe cardiovascular events. In this review, we outline recent advances in multidisciplinary research concerning Ca²⁺ signaling in VSMCs and ECs, with an emphasis on the mechanisms underlying functional and structural vascular remodeling.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"44 1","pages":"50"},"PeriodicalIF":0.0,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11673324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell fusion dynamics: mechanisms of multinucleation in osteoclasts and macrophages.","authors":"Hideaki Sabe, Yasuhito Yahara, Masaru Ishii","doi":"10.1186/s41232-024-00360-3","DOIUrl":"10.1186/s41232-024-00360-3","url":null,"abstract":"<p><p>Cell-cell fusion is a vital biological process where the membranes of two or more cells merge to form a syncytium. This phenomenon is critical in various physiological and pathological contexts, including embryonic development, tissue repair, immune responses, and the progression of several diseases. Osteoclasts, which are cells from the monocyte/macrophage lineage responsible for bone resorption, have enhanced functionality due to cell fusion. Additionally, other multinucleated giant cells (MGCs) also arise from the fusion of monocytes and macrophages, typically during chronic inflammation and reactions to foreign materials such as prostheses or medical devices. Foreign body giant cells (FBGCs) and Langhans giant cells (LGCs) emerge only under pathological conditions and are involved in phagocytosis, antigen presentation, and the secretion of inflammatory mediators. This review provides a comprehensive overview of the mechanisms underlying the formation of multinucleated cells, with a particular emphasis on macrophages and osteoclasts. Elucidating the intracellular structures, signaling cascades, and fusion-mediating proteins involved in cell-cell fusion enhances our understanding of this fundamental biological process and helps identify potential therapeutic targets for disorders mediated by cell fusion.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"44 1","pages":"49"},"PeriodicalIF":0.0,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11600601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142741812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}