Cell Communication and Signaling最新文献

{"title":"Ca²⁺-dependent pathways controlled by Piezo1 activity in human erythroid progenitor cell line: focus on KCa3.1 channels, ANO6 lipid scramblases and pannexins-1.","authors":"Anastasia V Sudarikova, Valeria Y Knyazeva, Irina O Vassilieva, Zuleikha M Rudneva, Vladislav I Chubinskiy-Nadezhdin","doi":"10.1186/s12964-026-03119-0","DOIUrl":"https://doi.org/10.1186/s12964-026-03119-0","url":null,"abstract":"<p><strong>Background: </strong>Piezo1 is a mechanosensitive Ca²⁺-permeable ion channel that plays a crucial role in the Ca²⁺ signaling processes of human red blood cells (RBCs). Ca²⁺ influx through Piezo1 controls the activity of various molecules that are crucial for RBC physiology and pathophysiology, including Ca²⁺-activated K⁺ channels of intermediate conductance (KCa3.1, or Gardos channels), ANO6 lipid scramblases and pannexins-1 (Panx1). Erythropoiesis, the differentiation of erythropoietic stem cells in the bone marrow to myeloid progenitor cells and then to mature (RBCs, is traditionally studied using different blood cell lines as models. Among them, K562 cells, a human chronic myeloid leukemia cell line, are multipotent progenitors of hematopoietic cells that can be differentiated along the erythroid lineage, thus making these cells an invaluable model for studying human erythropoiesis. As K562 is an immortalized cell line obtained from a specific donor, the putative differences in the relevant pathways between K562 cells and human RBCs should be identified and taken into account. Here, we aimed to reveal and compare the functional interactions between Ca²⁺ influx through Piezo1 and Gardos channel, ANO6 and Panx1 activities in K562 cells and RBCs.</p><p><strong>Methods: </strong>Database analysis was performed to confirm the expression of genes of interest and putative mutations in K562 cells. Mutations were confirmed using Sanger sequencing. Piezo1 activity in the plasma membrane was stimulated by a selective Piezo1 agonist, Yoda1. KCa3.1 activation was detected using light microscopy and single-channel patch-clamp analysis. PS exposure was detected by AnV fluorescent staining. Presence of Panx1 was shown using RT-PCR, Western Blot and immunofluorescence. K562 differentiation was induced by cytarabine-hemin treatment and confirmed by a benzidine test. Panx1 activation was probed using dye uptake assay and whole-cell patch-clamp recordings.</p><p><strong>Results: </strong>We found that, similar to RBCs, both Piezo1-KCa3.1 and Piezo1-ANO6 functional links are present in K562 cells, whereas the Piezo1-Panx1 axis is not functional because Panx1 cannot be activated by Ca²⁺ in this cell line.</p><p><strong>Conclusions: </strong>Thus, the physiologically relevant pathways associated with Ca²⁺-induced Panx1 activity in K562 cells may significantly differ from those that are functional in human RBCs.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149247692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging of hair follicle stem cells and their niche: mechanisms and regenerative therapeutic strategies.","authors":"Siqi Xu, Jiming Guo, Ying Kang, Qinjing Wang, Yue Ming, Weixing Chen, Min Wang, Zhijie Huang, Yisheng Huang, Bo Jia","doi":"10.1186/s12964-026-03086-6","DOIUrl":"10.1186/s12964-026-03086-6","url":null,"abstract":"<p><p>Hair follicles (HFs) are vital skin appendages that perform fundamental functions including protection, thermoregulation, and sensation. Orchestrated by hair follicle stem cells (HFSCs), HFs undergo cyclic regeneration throughout the lifespan. However, during chronological aging, this mini-organ experiences progressive physiological decline, clinically characterized by a marked reduction in hair density and hair graying due to pigmentation dysfunction. This aging process involves HFSC exhaustion accompanied by diminished regenerative potential and differentiation capacity, leading to degenerative changes in the bulge architecture. Concurrently, the niche supporting HFSC homeostasis undergoes multi-dimensional and systemic degradation. This niche deterioration disrupts the delicate balance between HFSC quiescence and activation, further impeding hair regeneration. In this review, we delineate the dynamic anatomical changes throughout the hair growth cycle and describe the alterations of HFSCs during aging. We specifically focus on the mechanisms underlying the multi-dimensional degradation of the HFSC niche at tissue, cellular, and molecular levels. Furthermore, we discuss various therapeutic strategies aimed at ameliorating HF aging, offering potential insights for future clinical translation in hair regeneration. Finally, we propose that integrating spatiotemporal high-resolution technologies with genomic data to further decipher the spatiotemporal behaviors of aging HFSCs and niche cells will facilitate the establishment of a robust mechanistic framework for HFSC and niche aging.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D chromatin structure remodelling in cancer.","authors":"Yang Liu, Minghua Wu","doi":"10.1186/s12964-026-03097-3","DOIUrl":"10.1186/s12964-026-03097-3","url":null,"abstract":"<p><p>Three-dimensional (3D) chromatin structure is crucial for gene regulation and cellular identity, with alterations in this structure being closely associated with tumor development. Although the research of tumor genomics has made significant progress in the past decade, the mechanism of 3D chromatin structure in tumorigenesis is not completely clear. Recent studies have shown that the distortion of chromatin spatial conformation has become one of the core factors driving normal cell carcinogenesis by changing the gene regulatory network. Abnormal high-order chromatin organization leads to abnormal activation of oncogenes or silencing of tumor suppressor genes. This 3D chromatin disorder has been confirmed to be directly related to the phenotypic plasticity of a variety of tumors. Therefore, the dynamic changes of 3D chromatin structure play a key role in the occurrence and development of tumors, especially for malignant tumors with difficult diagnosis and lack of treatment. This article provides an overview of hierarchical alterations in cancer 3D chromatin structure, the mechanisms governing these changes, recent advances in detection technologies, and emerging therapeutic strategies. The unique 3D chromatin variation pattern in cancers may become a new biomarker and provide a theoretical basis for epigenetic therapy targeting chromatin spatial organization. In the future, integrating multi-omics data to develop specific drugs for key nodes of the 3D chromatin and establishing an early diagnosis system based on spatial chromatin characteristics will become an important direction to break through the bottleneck of cancer treatment.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ADAM12 in a stromal-checkpoint framework: integrating tumor microenvironment remodeling and therapy resistance in solid tumors.","authors":"Shaochun Liu, Jian Xu, Han Zhang, Yuhan Tang, Xiaoxi Han, Wenjing Xiong, Linlin Fan, Chang Su, Zhiqi Sui, Wenhui Zhao","doi":"10.1186/s12964-026-03103-8","DOIUrl":"10.1186/s12964-026-03103-8","url":null,"abstract":"<p><p>The tumor microenvironment (TME) is now understood as an active regulator of therapeutic vulnerability. In this Review, we use an integrative stromal-checkpoint framework, informed by published stromal and fibroblast checkpoint studies, to describe stromal programs that couple extracellular matrix (ECM) remodeling, metabolic stress, vascular dysfunction, and immune exclusion into treatment-resistant tumor ecologies. We focus on a disintegrin and metalloproteinase 12 (ADAM12) because ADAM12-high or ADAM12-positive tumor-stromal states have been linked to collagen-rich desmoplasia, mechanotransduction, hypoxia-associated stress, lactate-associated acidosis, immune-excluded spatial organization, and therapy resistance in solid tumors. Evidence spans fibroblast, mesenchymal stromal-cell, and tumor-cell perturbation studies; mechanistic substrate and signaling analyses; spatial and clinical datasets; and broader tissue-level immune contexts relevant to lymphatic drainage, tumor-draining lymph node (TDLN) priming, tissue-resident immune cells, and ILC2/type 2 immune programs. Across these evidence layers, ADAM12 emerges as an isoform-aware and cell-of-origin-dependent marker, amplifier, and context-dependent candidate target for selected high-barrier tumor states. We discuss how ADAM12-informed biomarkers, spatial barrier profiling, and stromal-priming strategies can support patient stratification and combination-therapy design. Overall, ADAM12-associated biology provides a useful model for examining how stromal resistance may be built, maintained, and therapeutically remodeled in selected tumor contexts.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13685229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149229200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of L1CAM from gastric epithelial cells and extracellular vesicles promotes Helicobacter pylori-driven cancer progression and invasiveness.","authors":"Supriya Samal, Smaran Banerjee, Abhisek Brahma, Prabin Bawali, Aranya Pal, Debashish Chakraborty, Indrajit Poirah, Gautam Nath, Sasmita Panda, Niranjan Rout, Shivaram P Singh, Saurabh Chawla, Duane T Smoot, Hassan Ashktorab, Asima Bhattacharyya","doi":"10.1186/s12964-026-03087-5","DOIUrl":"10.1186/s12964-026-03087-5","url":null,"abstract":"<p><strong>Background: </strong>Helicobacter pylori (Hp) infection is a major risk factor for gastric cancer (GC). While Hp-driven alterations in host signaling have been widely studied, the contribution of extracellular vesicles (EVs) to this process remains largely unexplored. Cell adhesion molecules play key roles in maintaining epithelial integrity and their dysregulation is often associated with malignant transformation. L1 cell adhesion molecule (L1CAM), a transmembrane protein involved in cell-cell interactions and signaling, has been implicated in cancer progression but its regulation in the context of Hp infection remains unclear. Here, we aimed to determine the relevance of L1CAM regulation and its EV-associated dynamics in Hp infection-induced GC.</p><p><strong>Methods: </strong>L1CAM status was assessed in Hp-positive gastric biopsy specimens by immunofluorescence microscopy and by western blotting of Hp-infected gastric epithelial cells (GECs). EVs from infected GECs were isolated and characterized. Functional assays, including proliferation, migration and xenograft studies were performed using infected or uninfected L1CAM-overexpressing as well as empty-vector cell-derived EVs. Integrin modulation by L1CAM was assessed by immunoblotting and microscopy in in vitro studies, patient samples and xenograft models using L1CAM-modulated cells. Epithelial-mesenchymal transition (EMT) markers, L1CAM proteolysis and inhibition studies were analyzed by immunoblotting to delineate the underlying molecular mechanisms.</p><p><strong>Results: </strong>Hp infection caused a marked loss of the full-length (FL) L1CAM in GECs and secreted GEC-EVs. A similar decrease was observed in Hp-positive GC tissues and plasma-derived EVs. Mechanistically, Hp-driven loss of FL-L1CAM resulted from the metalloproteinase ADAM10-mediated cleavage and was accompanied by the appearance of L1CAM fragments in infected cells or their EVs. EVs derived from infected cells significantly enhanced proliferation and migration of non-cancerous GECs in vitro as well as promoted tumor growth in vivo. In contrast, EVs from uninfected cells attenuated these malignant traits, suggesting that Hp-associated proteolytic depletion of FL-L1CAM fosters a tumor-promoting phenotype. Additionally, loss of FL-L1CAM induced EMT and selectively decreased αVβ1 integrin across infected cells, patient biopsies and xenograft tissues, defining a distinct Hp-driven L1CAM-ADAM10-αVβ1 signaling axis.</p><p><strong>Conclusion: </strong>Hp-induced proteolytic cleavage of L1CAM represents a distinct molecular signature of Hp-associated GC. FL-L1CAM-depleted EV may serve as a promising minimally invasive biomarker in Hp-driven gastric carcinogenesis.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trophoblast derived extracellular vesicles trigger secondary vesicle release from endometrial epithelial cells.","authors":"Subhashini Muhandiram, Seyed Omid Reza Mousavi, Suranga Kodithuwakku, Kasun Godakumara, Sergei Kopanchuk, Ago Rinken, Getnet Midekessa, Alireza Fazeli","doi":"10.1186/s12964-026-03096-4","DOIUrl":"10.1186/s12964-026-03096-4","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are emerging mediators of cellular communication, carrying bioactive molecules that can alter the function of recipient cells. Yet, how these signals are recognized and interpreted by recipient cells remains unclear. For communication to be effective, signals must reach the right cells at the right time, suggesting that EVs likely target specific cells, an aspect often overlooked in mechanistic studies.In this study, we used an in vitro embryo implantation model consisting of JAr (trophoblast) and RL95-2 (endometrial) cells to explore targeted communication in a physiologically relevant context. Our previous findings showed that JAr-derived EVs specifically induce rapid secretion of milk fat globule epidermal growth factor-8 (MFGE8) from RL95-2 cells. Using MFGE8 as a functional readout, we further investigated the underlying mechanisms of EV mediated targeted cell communication.We found that RL95-2 responses to JAr EVs depend on clathrin-mediated endocytosis and endosomal acidification. Moreover, Rab27a-dependent secondary vesicle release contributed to increased MFGE8 secretion in endometrial cells. Importantly, optimal EV activity required precise pairing between EVs and recipient cells, indicating that EV-triggered vesicle release is not merely a recycling process. Finally, recipient cell stress disrupted vesicle release and impaired responses to EV signals. By combining this in vitro model with MFGE8 as a rapid functional readout, we highlight a natural mechanism of targeted EV communication.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13681822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small extracellular vesicles are the key players in ochratoxin A-induced kidney toxicity.","authors":"Sourin Adhikary, Indra Dev, Abu Rafay, Pankaj R Jagdale, Sukhveer Singh, Anjaneya Ayanur, Kausar Mahmood Ansari","doi":"10.1186/s12964-026-03023-7","DOIUrl":"10.1186/s12964-026-03023-7","url":null,"abstract":"<p><strong>Background: </strong>Despite growing evidence of ochratoxin A (OTA)-induced kidney toxicity, the underlying mechanisms remain elusive. Emerging evidence suggests that small extracellular vesicles (sEVs) act as mediators of intercellular communication to recipient cells during various physiological and pathological conditions. Given the distinctive properties of sEVs, it is hypothesized that OTA-induced sEVs might mediate the OTA-induced kidney pathogenesis.</p><p><strong>Methods: </strong>To explore the involvement of sEVs in OTA-induced kidney toxicity, sEVs were isolated and characterized from OTA-exposed rat kidney epithelial cells (NRK52E). Later, these sEVs were used to treat NRK52E cells and Wistar rats to assess the impact of OTA-induced sEVs on kidney toxicity. Label-free proteomics was also performed on OTA-induced sEVs, and key proteins were identified and validated. The biodistribution of sEVs in rats was also assessed using live imaging. The role of validated protein/s in kidney toxicity was further confirmed via a gene silencing and overexpression study.</p><p><strong>Results: </strong>OTA exposure increased sEV secretion into conditioned media of NRK52E cells and into the urine of Wistar rats. Interestingly, we found that OTA-induced sEVs cause similar kidney toxicity in vitro and in vivo systems as OTA exposure, and blocking of sEV secretion markedly alleviated OTA-mediated kidney toxicity. Proteomics analysis identified annexin A2 and fibrinogen-ɣ as common proteins detected in sEVs derived from OTA-exposed NRK52E cells or rat urine. However, immunoblotting validated that annexin A2 was the only sEV-associated protein, expressed significantly in both NRK52E and rat urine following OTA exposure. Notably, silencing of annexin A2 attenuated the ability of OTA-induced sEVs to cause kidney toxicity, whereas overexpression exacerbates it.</p><p><strong>Conclusions: </strong>Our findings identify the annexin A2-enriched sEVs as key mediators of OTA-induced kidney toxicity. Annexin A2, along with other kidney injury markers, offers a promising non-invasive translational biomarker for early detection and monitoring of OTA-induced kidney toxicity.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation in cancer: a new frontier in metabolic-epigenetic regulation and clinical practice.","authors":"Yihan Zhang, Lan Chen, Yaxi Qin, Ying Wang, Xi Liu, Minghui Zhang, Jing Tang","doi":"10.1186/s12964-026-03085-7","DOIUrl":"10.1186/s12964-026-03085-7","url":null,"abstract":"<p><p>The discovery of lysine lactylation (Kla) redefines lactate from a passive glycolytic by-product into a bioactive metabolic mediator that directly links cellular metabolism to epigenetic regulation. This emerging post-translational modification dynamically alters histone and non-histone proteins, thereby reconfiguring gene expression programs and immune responses within the tumor microenvironment (TME). It consequently promotes core malignant phenotypes including uncontrolled proliferation, epithelial-mesenchymal transition (EMT), metastatic dissemination, and resistance to chemotherapy, radiotherapy, and immune checkpoint blockade. Specific epigenetic signatures, notably histone H3K18la and H4K12la marks, serve as transcriptional anchors for oncogenic pathways across multiple cancer types. Multi-omics analyses have further yielded Kla-associated gene profiles with the potential to refine prognostic stratification and drug-target identification. These findings establish Kla as a central axis in tumor-associated metabolic-epigenetic crosstalk. Effective clinical application of KLAsKla biomarkers requires resolving technical detection limits and addressing the spatiotemporal heterogeneity that currently constrains machine learning-based prognostic models. Overcoming these bottlenecks is contingent upon leveraging advanced technologies such as single-cell multi-omics and spatial transcriptomics. This review characterizes the emerging roles of Kla in tumor metabolism, providing a framework for its future application as a diagnostic and therapeutic cornerstone in precision oncology.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13682118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S100a4 mediated peritoneal B1 lymphocytes play a critical role in host protection against helminth infection.","authors":"Fei Guan, Xi Luo, Yanmei Huang, Jiang Chang, Ju Liu, Wenwen Zheng, Jinyuan Zhang, Yiyan Gong, Heng Gu, Yi Wang, Yonggui Wu, Wenqi Liu, Jiahui Lei, Chaohong Liu","doi":"10.1186/s12964-026-03091-9","DOIUrl":"10.1186/s12964-026-03091-9","url":null,"abstract":"<p><strong>Background: </strong>Trichinellosis is a globally prevalent parasitic disease caused by infection of Trichinella spiralis. B1 cells are critically involved in immune defense against multiple parasitic infections, yet their functional role in trichinellosis remains uncharacterized.</p><p><strong>Methods: </strong>Wild-type, Btk conditional knockout and S100a4 knockout mice were used to construct the infection model of T. spiralis. The proportions and BCR signaling of peritoneal B1 cells in mice infected with T. spiralis were detected with flow cytometry and immunofluorescence. RNA sequencing was applied to analyze the possible mechanisms of B1 cell activation. ELISA was used to detect the production of antibodies.</p><p><strong>Results: </strong>Peritoneal B1 cells exhibited obvious accumulation with enhanced B cell receptor (BCR) signaling at the muscle phase of murine T. spiralis infection. B1 cell deficiency impaired host immune responses against T. spiralis at the muscle stage, confirming the essential contribution of B1 cells to anti-trichinella immunity. RNA sequencing analysis revealed significant upregulation of S100A4 in peritoneal B1 cells following infection. Mechanistically, S100A4 regulated the biological functions of peritoneal B1 cells through modifying cell relocation, BCR signaling, and antibody production.</p><p><strong>Conclusions: </strong>Our findings reveal a previously unrecognized role of S100A4-mediated B1 cell responses in host defense against T. spiralis infection. The data provide new mechanistic insights into the immune regulation of trichinellosis.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148889386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian clock and its potential as a therapy for ischemic heart disease.","authors":"Yiran Wang, He Wang, Ning Liu, Jiayi Zhang, Bin Liu","doi":"10.1186/s12964-026-03073-x","DOIUrl":"10.1186/s12964-026-03073-x","url":null,"abstract":"<p><p>According to an epidemiological survey, myocardial infarction, ischemia-reperfusion injury, and aortic rupture usually occur in the morning and summer and are characterized by more severe symptoms and poorer prognosis. The occurrence, development, treatment difficulties, and poor prognosis of ischemic heart disease are closely related to circadian rhythm disorders and the abnormal transcription of circadian clock genes. Normal circadian rhythms regulate neurohumoral regulation and energy metabolism, thereby playing a protective or modulatory role in ischemic heart disease (IHD). HIF1α links the IHD and circadian signaling pathways through the hypoxia response element (HRE) and Per-Arnt-Sim (PAS) domains in gene promoters and enhancers.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"24 1","pages":""},"PeriodicalIF":11.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13682045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}