Inflammation and regeneration最新文献

{"title":"Potential therapeutic applications of stem cells in animal models of ocular affections.","authors":"Taghreed A Hassan, Yara S Abouelela, Hamdy Rizk, Ayman Tolba","doi":"10.1186/s41232-025-00380-7","DOIUrl":"10.1186/s41232-025-00380-7","url":null,"abstract":"<p><strong>Background: </strong>Ocular affections are serious damage to the ocular tissue that results in impaired vision or blindness. Cell-based therapies are a potentially effective therapeutic technique that entails using stem-like precursor cells to induce differentiation of specific cell types and implanting the cells to improve vision in the affected tissue area.</p><p><strong>Methods: </strong>Numerous clinical trials were started to investigate the potential benefits of stem cells for treating ocular affections, based on several encouraging findings from the preclinical research. Following our review, data were collected from various databases, \"Google Scholar, Springer, Elsevier, Egyptian Knowledge Bank, ProQuest, and PubMed\" using different keywords such as corneal ulcer, retinopathy, glaucoma, ocular regeneration, and stem cells to investigate the various methods for regeneration of ocular affections. The data were obtained and analyzed.</p><p><strong>Results: </strong>This review includes tables that show all types of stem cells that were used to treat ocular diseases, such as mesenchymal stem cells (MSCs), hematopoietic stem cells, neural stem cells, embryonic stem cells, and induced pluripotent stem cells. The several characteristics of MSCs that aid in the restoration and regeneration of injured ocular tissue are outlined in this paper, along with their potential applications in the management of ocular degenerative diseases, as determined by physical, histological, immunohistochemical, and biochemical evaluations. Finally, our review highlights the most effective regenerative strategies that assist in rapid ocular regeneration in a variety of animal models, including mice, rats, rabbits, and goats.</p><p><strong>Conclusion: </strong>With the promising results of multiple preclinical studies, stem cell therapy is still a great choice for treating ocular degenerative illnesses. To improve the clinical outcomes, co-transplantation of two or more cell types may be a possibility for future treatment alternatives.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"23"},"PeriodicalIF":0.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144683894","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":"Mutation of the histone demethylase Gasc1 causes ASD-like symptoms in mice.","authors":"Tetsushi Kagawa, Yuhei Yamaguchi, Yasuhiro Kokubu, Genki Sudo, Aoi Ebisawa, Satoko Hattori, Keizo Takao, Kohtarou Konno, Naomi Nakagata, Takafumi Inoue, Masahiko Watanabe, Johji Inazawa, Tsuyoshi Miyakawa, Tetsuya Taga","doi":"10.1186/s41232-025-00374-5","DOIUrl":"10.1186/s41232-025-00374-5","url":null,"abstract":"<p><strong>Background: </strong>Genomic analyses of psychiatric disorders, including autism spectrum disorder (ASD), have revealed many susceptibility genes, suggesting that such disorders may be caused by multiple factors. In this sense, it has long been a question whether there is an abnormal genetic status that comprehensively explains the pathogenesis of neuropsychiatric disorders or a\"promising upstream treatment target\"that normalizes symptoms.</p><p><strong>Methods: </strong>To address this question, we provide important clues with respect to GASC1 (JMJD2 C/KDM4 C), which is a histone demethylase that prominently targets trimethylated histone H3 at lysine 9 (H3 K9 me3). Gasc1 hypomorphic mutant mice were analyzed using molecular biological, biochemical, behavioral battery tests, histological, and electrophysiological techniques.</p><p><strong>Results: </strong>Mice homozygous for a hypomorphic mutation in Gasc1 exhibited abnormal behaviors, including hyperactivity, stereotyped behaviors, and impaired learning and memory, which are reminiscent of those of human psychiatric disorders. Electrophysiological studies of hippocampal slices revealed decreased paired-pulse facilitation and enhanced long-term potentiation, suggesting synaptic dysfunction in the mutants. Increased dendritic spine density in CA1 neurons was also detected in the mutants. Intriguingly, genetic linkage studies of human ASD have mapped a susceptibility locus on chromosome 9p24.1, which contains 78 genes, including the GASC1 gene.</p><p><strong>Conclusion: </strong>Taken together, our data suggest that histone demethylation plays a pivotal role in normal brain development and higher-order brain functions in both mice and humans.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"22"},"PeriodicalIF":0.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602621","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":"The impact of T cells on immune-related liver diseases: an overview.","authors":"Yuzo Koda, Ryosuke Kasuga, Nobuhito Taniki, Takanori Kanai, Nobuhiro Nakamoto","doi":"10.1186/s41232-025-00387-0","DOIUrl":"10.1186/s41232-025-00387-0","url":null,"abstract":"<p><p>The liver presents a unique immune system. Liver diseases are closely associated with the immune system. Disruption of the tightly regulated balance between immune activation and tolerance induction leads to the development and worsening of immune-related liver diseases. T cells play diverse crucial roles in the immune system, and they have long been known to induce inflammation through direct tissue damage by effector molecules and the recruitment of effector cells via chemokines. Additionally, T cells interact with B cells to induce autoantibodies, promoting tissue inflammation and dysfunction through the deposition of IgG and immune complexes in the tissues. Recent advances in omics technologies, including single-cell RNA sequencing and spatial transcriptomics, have elucidated the role of T cells in the progression and recovery of liver fibrosis. Moreover, comprehensive and unbiased information can now be obtained from small samples of human and mouse tissues, which advances our understanding of tissue-specific functions of T cells, including resident memory T cells, peripheral helper T cells, and tissue Tregs. However, significant unmet needs remain in the fields of immune-related liver diseases. In this review, we discuss the T cell biology and its role in autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), primary biliary cholangitis (PBC), and metabolic-associated steatohepatitis (MASH), which are non-viral liver diseases exhibiting a strong involvement of immunity and inflammation. Furthermore, the latest therapeutic concepts for the diseases and associated drugs targeting T cells have been overviewed.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"21"},"PeriodicalIF":0.0,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144565574","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":"The influence of the choroid plexus on brain function: beyond its role in cerebrospinal fluid production.","authors":"Sayako Katada, Kelren S Rodrigues, Kinichi Nakashima","doi":"10.1186/s41232-025-00386-1","DOIUrl":"10.1186/s41232-025-00386-1","url":null,"abstract":"<p><p>The choroid plexus (ChP) is a highly vascularized tissue located within the brain ventricles. Traditionally recognized for its primary role in cerebrospinal fluid (CSF) production, recent research has unveiled a far more complex and dynamic picture of the ChP's contributions to brain health and homeostasis. The ChP is composed of tight-junction-bound epithelial cells and the underlying stroma-rich fenestrated capillaries of blood vessels. This unique architecture creates a barrier between the peripheral blood and CSF, regulating the brain's internal environment. The discovery that CSF enters the brain parenchyma via the perivascular space, coupled with the identification of a functional brain lymphatic system linked to CSF turnover, further highlights the ChP as a gatekeeper of waste clearance and fluid homeostasis. This review will cover the development and histology of ChP, focusing on the dynamic response of the blood-CSF barrier in the context of systemic inflammation, a process whose molecular mechanisms have recently been elucidated.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"20"},"PeriodicalIF":0.0,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12219057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556258","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⁺ microdomain-based excitation-transcription coupling in cardiac myocytes and vascular smooth muscle cells.","authors":"Tsukasa Koide, Wayne R Giles, Rubii Kondo, Yuji Imaizumi, Hisao Yamamura, Yoshiaki Suzuki","doi":"10.1186/s41232-025-00384-3","DOIUrl":"10.1186/s41232-025-00384-3","url":null,"abstract":"<p><p>Ca²⁺ signals play a crucial role in maintaining cardiovascular homeostasis, including regulation of the heartbeat, blood pressure, and adaptation to changes in the external environment. Conversely, abnormal Ca²⁺ signaling is often involved in the onset and progression of cardiovascular diseases, such as cardiac hypertrophy, heart failure, arteriosclerosis, and hypertension. In excitable cells, such as cardiac myocytes and vascular smooth muscle cells (VSMCs), membrane depolarization, and the subsequent elevation of cytosolic Ca²⁺ concentration ([Ca²⁺]_cyt) via voltage-dependent Ca²⁺ channels (VDCCs) cause muscle contraction, which is known as excitation-contraction coupling (E-C coupling). Elevated [Ca²⁺]_cyt can also activate Ca²⁺-dependent enzymes, in some cases leading to changes in gene expression patterns and contributing to long-term cellular responses. This mechanism is referred to as excitation-transcription coupling (E-T coupling), and it is involved in both the adaptive and pathological responses of the cardiovascular system to chronic stimulation. Specific intracellular regions, known as Ca²⁺ microdomains, exhibit localized increases in [Ca²⁺]_cyt. Such localized Ca²⁺ signaling is now known to be one of the molecular mechanisms controlling the diversity of Ca²⁺ responses. These Ca²⁺ microdomains are often formed by complexes consisting of Ca²⁺ channels and downstream Ca²⁺-dependent enzymes localized by scaffolding proteins. This review outlines some of the molecular mechanisms and roles of Ca²⁺ microdomain-based E-T coupling in cardiac myocytes and VSMCs. First, we discuss the major molecular components that are essential for functional Ca²⁺ microdomains. For example, VDCC (Ca_V1.2 channel), ryanodine receptor (RyR), Ca²⁺-dependent enzymes (Ca²⁺/CaM-dependent kinase [CaMK], calcineurin [CaN], and calpain), and scaffolding proteins (A-kinase anchoring proteins [AKAPs], caveolin, and junctophilin). Next, we discuss the roles of Ca²⁺ microdomain-based E-T coupling in physiological and pathophysiological remodeling in cardiac myocytes and vascular smooth muscle cells.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"19"},"PeriodicalIF":0.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478274","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":"Genetic deletion of microsomal prostaglandin E synthase-1 promotes imiquimod-induced psoriasis in mice.","authors":"Fumiaki Kojima, Yuka Hioki, Miori Sumida, Yoshiko Iizuka, Hitoshi Kashiwagi, Kei Eto, Shiho Arichi, Shotaro Maehana, Makoto Kubo, Haruhito A Uchida, Takafumi Ichikawa","doi":"10.1186/s41232-025-00385-2","DOIUrl":"10.1186/s41232-025-00385-2","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a chronic inflammatory disease associated with abnormalities in the immune system. Microsomal prostaglandin E synthase-1 (mPGES-1), a terminal enzyme for prostaglandin (PG) E₂ biosynthesis, is highly expressed in the skin of psoriasis patients. However, the detailed role of mPGES-1 in psoriasis remains unclear. In the present study, we aimed to investigate the role of mPGES-1 in psoriasis-like skin inflammation induced by imiquimod (IMQ), a well-established model of psoriasis.</p><p><strong>Methods: </strong>Psoriasis was induced in mPGES-1-deficient (mPGES-1^-/-) and wild-type (WT) mice by administering IMQ for 6 days. Psoriasis was evaluated based on the scores of the macroscopic symptoms, including skin scaling, thickness, and redness, and on the histological features. The skin expression of mPGES-1 was determined by real-time polymerase chain reaction and Western blotting. The impact of mPGES-1 deficiency on T-cell immunity was determined by flow cytometry and γδ T-cell depletion in vivo with anti-T-cell receptor (TCR) γδ antibody.</p><p><strong>Results: </strong>The inflamed skin of mPGES-1^-/- mice showed severe symptoms after the administration of IMQ. Histological analysis further showed significant exacerbation of psoriasis in mPGES-1^-/- mice. In WT mice, the mPGES-1 expression was highly induced at both mRNA and protein levels in the skin, and PGE₂ increased significantly after IMQ administration, while the PGE₂ production was largely abolished in mPGES-1^-/- mice. These data indicate that mPGES-1 is the main enzyme responsible for PGE₂ production in the skin. Furthermore, the lack of mPGES-1 increased the numbers of IL-17A-producing γδ T cells in the skin with IMQ-induced psoriasis, and γδ T-cell depletion resulted in a reduction of the facilitated psoriasis symptoms under the condition of mPGES-1 deficiency.</p><p><strong>Conclusions: </strong>Our study results demonstrate that mPGES-1 is the main enzyme responsible for skin PGE₂ production, and that mPGES-1 deficiency facilitates the development of psoriasis by affecting the development of T-cell-mediated immunity. Therefore, mPGES-1 might impact both skin inflammation and T-cell-mediated immunity associated with psoriasis.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"18"},"PeriodicalIF":0.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12142878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251579","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":"Innate immune memory in macrophage differentiation and cardiovascular diseases.","authors":"Yukiteru Nakayama, Katsuhito Fujiu","doi":"10.1186/s41232-025-00382-5","DOIUrl":"10.1186/s41232-025-00382-5","url":null,"abstract":"<p><p>Innate immune memory (trained immunity) refers to the ability of innate immune cells, such as monocytes and macrophages, to retain a long-term imprint of a prior stimulus through epigenetic and metabolic adaptations, enabling amplified responses upon restimulation. Recent studies have classified innate immune memory into central and peripheral types. Central innate immune memory originates in hematopoietic stem cells (HSCs) within the bone marrow, where epigenetic reprogramming generates a sustained inflammatory bias, contributing to chronic diseases such as atherosclerosis, heart failure, and stroke. Peripheral innate immune memory occurs in monocytes or macrophages that acquire heightened responsiveness after repeated exposure to stimuli in peripheral tissues. This review explores the mechanisms underlying both central and peripheral innate immune memory, their roles in chronic inflammatory diseases, focusing on cardiovascular diseases, and potential strategies to target innate immune memory for therapeutic purposes. Advancing the understanding of these processes could facilitate the development of novel approaches to control inflammatory diseases and immune-related disorders.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"17"},"PeriodicalIF":0.0,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12131520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217944","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":"Unraveling the complex role of microglia in Alzheimer's disease: amyloid β metabolism and plaque formation.","authors":"Sho Takatori, Mayuna Kondo, Taisuke Tomita","doi":"10.1186/s41232-025-00383-4","DOIUrl":"10.1186/s41232-025-00383-4","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is characterized by amyloid β (Aβ) accumulation in the brain. Recent genome-wide association studies have identified numerous AD risk genes highly expressed in microglia, highlighting their potential role in AD pathogenesis. Although microglia possess phagocytic capacity and have been implicated in Aβ clearance, accumulating evidence suggests their contribution to AD pathogenesis is more complex than initially anticipated.</p><p><strong>Main body: </strong>This review synthesizes current knowledge on microglial Aβ metabolism in AD, reconciling conflicting data from various studies. We examine evidence supporting the role of microglia in Aβ clearance, including studies on AD risk genes like TREM2 and their impact on microglial phagocytosis. Conversely, we explore findings that challenge this view, such as microglial depletion experiments resulting in unchanged or decreased Aβ accumulation. We propose that the contribution of microglia to Aβ metabolism is context-dependent, varying with disease progression, genetic background, and experimental conditions. Notably, microglia may promote parenchymal amyloid accumulation in early disease stages, while this accumulation-promoting effect may diminish in later stages. We discuss potential mechanisms for this paradoxical effect, including intracellular Aβ aggregation and release of pro-aggregation factors. Additionally, we explore the interplay between microglia-mediated Aβ metabolism and other clearance pathways, such as the glymphatic system, highlighting a potential compensatory relationship between parenchymal amyloid deposition and cerebral amyloid angiopathy.</p><p><strong>Conclusion: </strong>Our review underscores the complex and dynamic role of microglia in AD pathogenesis. Understanding the stage-specific functions of microglia in Aβ metabolism is crucial for developing targeted interventions. Future research should focus on elucidating the mechanisms of microglial functional changes throughout disease progression and determining the pathological significance of these changes. Exploring potential therapeutic strategies that selectively enhance beneficial microglial functions while mitigating their detrimental effects remains an important goal.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"16"},"PeriodicalIF":0.0,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12123843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188722","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":"From bench to bedside: the role of gastrointestinal stem cells in health and disease.","authors":"Xiaopeng Bai, Eikichi Ihara, Yoshimasa Tanaka, Yosuke Minoda, Masafumi Wada, Yoshitaka Hata, Mitsuru Esaki, Haruei Ogino, Takatoshi Chinen, Yoshihiro Ogawa","doi":"10.1186/s41232-025-00378-1","DOIUrl":"10.1186/s41232-025-00378-1","url":null,"abstract":"<p><p>The gastrointestinal (GI) tract constitutes a sophisticated system integral to digestion, nutrient absorption, and overall health, with its functionality predominantly hinging on the distinctive properties of diverse stem cell types. This review systematically investigates the pivotal roles of stem cells across the esophagus, stomach, small intestine, and colon, emphasizing their crucial contributions to tissue homeostasis, repair mechanisms, and regeneration. Each segment of the GI tract is characterized by specialized stem cell populations that exhibit distinct functional attributes, highlighting the necessity for tailored therapeutic approaches in the management of gastrointestinal disorders.Emerging research has shed light on the functional heterogeneity of GI stem cells, with ISCs in the small intestine displaying remarkable turnover rates and regenerative potential, whereas colonic stem cells (CSCs) are essential for the preservation of the colonic epithelial barrier. The intricate interplay between stem cells and their microenvironment-or niche-is fundamentally important for their functionality, with critical signaling pathways such as Wnt and Notch exerting substantial influence over stem cell behavior. The advent of organoid models derived from GI stem cells offers promising avenues for elucidating disease mechanisms and for the preclinical testing of novel therapeutic interventions.Despite notable advancements in foundational research on GI stem cells, the translation of these scientific discoveries into clinical practice remains limited. As of 2025, Japan's clinical GI disease guidelines do not endorse any stem cell-based therapies, underscoring the existing disconnect between research findings and clinical application. This scenario accentuates the urgent need for sustained efforts to bridge this divide and to cultivate innovative strategies that synergize stem cell technology with conventional treatment modalities.Future investigations should be directed toward unraveling the mechanisms that underpin stem cell dysfunction in various gastrointestinal pathologies, as well as exploring combination therapies that harness the regenerative capacities of stem cells in conjunction with immunomodulatory treatments. By fostering collaborative endeavors between basic researchers and clinical practitioners, we can deepen our understanding of GI stem cells and facilitate the translation of this knowledge into effective therapeutic interventions, ultimately enhancing patient outcomes in gastrointestinal diseases.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"15"},"PeriodicalIF":0.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176252","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":"CD157⁺ vascular endothelial cells derived from human-induced pluripotent stem cells have high angiogenic potential.","authors":"Ami Takii, Yukika Tanabe, Wenting Li, Hiroki Shiomi, Akane Inoue, Fumitaka Muramatsu, Weizhen Jia, Nobuyuki Takakura","doi":"10.1186/s41232-025-00379-0","DOIUrl":"https://doi.org/10.1186/s41232-025-00379-0","url":null,"abstract":"<p><strong>Background: </strong>We previously reported that a vascular endothelial stem cell population resides in pre-existing blood vessels in mice and may contribute to vascular endothelial cells in liver injury or hind limb ischemia models in the long-term. However, whether such stem cells exist in humans and can differentiate specifically into vascular endothelial cells have not been determined. We hypothesized that CD157⁺ vascular endothelial cells in humans may also possess high angiogenic potential.</p><p><strong>Methods: </strong>First, human-derived induced pluripotent stem cells were differentiated into vascular endothelial cells and the expression of CD157 was monitored during the differentiation process. We found that CD157 emerged 11 days after the induction of differentiation, peaked at 14 days, and then declined by 24 days. We also evaluated blood vessel formation by 14- and 24-day-old vascular endothelial cells.</p><p><strong>Results: </strong>It was found that 14-day-old cells, when CD157 expression was at its peak, formed more blood vessels than 24-day-old cells.</p><p><strong>Conclusion: </strong>These results suggest that vascular endothelial cells expressing CD157 have high angiogenic potential and may exist as vascular endothelial stem cells.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"45 1","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082543","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}