Journal of Cell Communication and Signaling最新文献

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148095347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148087966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imperatorin ameliorates myocardial ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress-mediated apoptosis via the PI3K/AKT/Nrf2 pathway.","authors":"Mingjun Han, Fan Yu, Huanhuan Li","doi":"10.1002/ccs3.70084","DOIUrl":"10.1002/ccs3.70084","url":null,"abstract":"<p><p>Endoplasmic reticulum stress (ERS) is a major event associated with myocardial ischemia-reperfusion injury (MIRI). Imperatorin (IMP) has cardioprotective effects, but its role in MIRI has not been reported. H9c2 cells were injured by the hypoxia/reoxygenation (H/R) method. The MIRI mouse model was prepared by coronary artery ligation and by using IMP, and the PI3K/AKT agonist 740 Y-P and inhibitor LY294002 were used for intervention. Cardiomyocyte apoptosis was determined through flow cytometry and TUNEL staining. Western blot, transmission electron microscopy, calcium assay kits, and Fluo-4 AM fluorescent probe were used to evaluate ERS and Ca²⁺ levels. In addition, the PI3K/AKT/Nrf2 pathway protein expressions were detected. IMP could significantly reduce cardiomyocyte apoptosis in H9c2 cells and myocardial tissue of MIRI mice, reduce ER swelling and damage, restore ER membrane structure, and reduce Ca²⁺ content and Caspase 12 and C/EBP homologous protein (CHOP) protein levels. IMP also increased p-PI3K and p-AKT proteins and the nuclear translocation of Nrf2 in H9c2 cells and myocardial tissue of MIRI mice. After IMP treatment combined with 740 Y-P intervention, the effect of IMP on improving cardiomyocyte apoptosis and ERS was further promoted, and the apoptosis rate, Ca²⁺ content, and caspase 12 and CHOP protein levels were significantly reduced. LY294002 weakened the improvement of IMP, and apoptosis and ERS levels increased significantly. IMP attenuated MIRI by inhibiting ERS and myocardial apoptosis through activating the PI3K/AKT/Nrf2 pathway.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":"e70084"},"PeriodicalIF":4.0,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148086366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A working model for CCN3 C-terminal domain-mediated transcriptional modulation of the plasminogen activation system.","authors":"Bernard Perbal","doi":"10.1002/ccs3.70083","DOIUrl":"10.1002/ccs3.70083","url":null,"abstract":"<p><p>Over the past 2 decades, major advances have contributed to the elucidation of the structural and biochemical bases underlying the biological activities attributed to CCN proteins. The concept that CCN proteins exhibit bifunctional \"moonlighting\" properties in both the extracellular matrix (ECM) and the cell nucleus has recently emerged. CCN proteins participate in dual signaling processes, integrating combinatorial interactions with regulatory ligands, cell surface receptors or associated co-receptors such as heparan sulfate proteoglycans (HSPGs), LRPs, TrkA, Notch, integrins, BMP-4, TGF-β, and FGFR2, as well as transcription factors in the nuclear compartment. In this manuscript, we propose an exploratory integrative model that brings together previously unassociated observations into a coherent framework. In this model, the C-terminal module, present in all CCN proteins except CCN5, is proposed to direct the formation of homo- and heterodimers, which constitute a fundamental level of transcriptional regulation.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":"e70083"},"PeriodicalIF":4.0,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13285853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148308270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148082098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between endoplasmic reticulum stress and mitochondrial homeostasis: A new perspective on ophthalmic disease treatment.","authors":"Luyang Jiang, Gongsang Cuomu, Sang Jijia, Yumei Yang, Jufen Liu, Yumin Tao","doi":"10.1002/ccs3.70080","DOIUrl":"10.1002/ccs3.70080","url":null,"abstract":"<p><p>Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are hallmarks of many ophthalmic diseases; however, they have traditionally been examined as isolated pathological processes. Recent evidence indicates that these organelles are inextricably coupled through mitochondria-endoplasmic reticulum contact sites, also known as mitochondria-associated membranes (MAMs), which coordinate Ca²⁺ signaling, lipid transfer, mitochondrial dynamics, redox balance, and cell death decisions. Consequently, dysregulated ER-mitochondria communication has emerged as a key vulnerability that links the cellular stress responses among diverse ocular tissues, including lens epithelial cells, retinal ganglion cells, the retinal pigment epithelium, and corneal endothelial cells. In this review, we summarize the recent advances involving the molecular architecture and regulatory function of ER-mitochondria crosstalk. We focus on how the unfolded protein response signaling, pathological MAM remodeling, Ca²⁺ dysregulation, and disrupted mitochondrial quality control collectively drive disease progression. By integrating evidence from cataract, glaucoma, diabetic retinopathy, age-related macular degeneration, and Fuchs endothelial corneal dystrophy, we reveal that these disorders are not driven by a uniform mechanism of organelle failure, but rather by the dominance of pathological nodes along the ER-mitochondria axis. We propose that ophthalmic diseases should be stratified based on these distinct failure nodes, which provides a mechanistic framework for developing therapeutics. Within this context, interventions targeting maladaptive ER stress, MAM destabilization, bioenergetic failure, or defective mitophagy should be considered complementary and context-dependent strategies. By reframing ophthalmic disorders as diseases of inter-organelle stress integration, this review positions the ER-mitochondria axis as a modifiable upstream determinant of ocular cell fate, which provides a foundation for stage-specific precision therapies.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70080"},"PeriodicalIF":4.0,"publicationDate":"2026-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13179842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147963866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATOX1 alleviates radiation-induced cardiac injury by modulating AMPK/NRF2 to inhibit myocardial oxidative stress and mitochondrial dysfunction.","authors":"Wen Deng, Li Su","doi":"10.1002/ccs3.70079","DOIUrl":"10.1002/ccs3.70079","url":null,"abstract":"<p><p>Radiation-induced heart disease (RIHD) is a myocardial lesion caused by radiation exposure, and its pathogenesis is closely associated with oxidative stress. ATOX1 has been demonstrated to regulate oxidative stress, but its mechanism in RIHD remains unclear. We analyzed ATOX1 expression (Western blot [WB], RT-PCR), cardiomyocyte proliferation (MTT, IF), apoptosis (TUNEL), AMPK signaling (WB, IF), and mitochondrial function (reactive oxygen species [ROS], mPTP, JC-1) in vitro. A thoracic irradiation model was used in cardiomyocyte-specific ATOX1 knockout mice. Tissue analysis included IHC for ATOX1, KI-67, p-AMPK, and assessment of myocardial injury (ELISA, RT-PCR, and Masson's staining). Irradiation significantly reduced cardiomyocyte proliferation and increased apoptosis. ATOX1 levels plummeted in irradiated cardiomyocytes, accompanied by mitochondrial ROS surges and disrupted integrity. Irradiation suppressed the AMPK/NRF2 axis, an effect reversed by ATOX1 overexpression. In mice, ATOX1 knockout exacerbated radiation-induced myocardial tissue damage. ATOX1 mitigates irradiation-induced cardiac damage by promoting mitochondrial and redox homeostasis in cardiomyocytes through AMPK/NRF2 pathway activation.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70079"},"PeriodicalIF":4.0,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13179142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147963892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148080392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte growth factor/c-Met signaling axis in human diseases: Mechanistic insights and therapeutic potential.","authors":"Hongqin Sun, Hao Shu, Qian Zhang, Jishan Zheng, Yunyan Ma, Dengwang Chen, Jidong Zhang, Tao Song","doi":"10.1002/ccs3.70075","DOIUrl":"10.1002/ccs3.70075","url":null,"abstract":"<p><p>Hepatocyte growth factor (HGF) is a multifunctional cytokine that activates the tyrosine kinase activity of its specific receptor, c-Met (mesenchymal-epithelial transition factor). This activation subsequently regulates downstream signaling pathways such as PI3K/Akt and Ras/MEK, ultimately mediating key biological processes including epithelial cell migration, proliferation, morphogenesis, and damaged tissue regeneration. Accumulating evidence indicates that the HGF/c-Met pathway is critical for embryonic development and tissue homeostasis. Dysregulation of this pathway-whether excessive activation or suppression-is closely associated with the pathogenesis of numerous human diseases. This review systematically synthesizes recent research data on the HGF/c-Met pathway and elucidates its disease-related mechanisms: it promotes malignant tumor progression, participates in viral infectious disease pathogenesis, facilitates tissue injury repair, and is implicated in diabetes mellitus and Alzheimer's disease. It further clarifies the pathway's fundamental biological functions, summarizes potential therapeutic strategies targeting this pathway (e.g., c-Met inhibitors, HGF antagonists, and microRNA-mediated regulation), and discusses challenges in clinical translation (e.g., poor target specificity and drug resistance), providing a theoretical reference for subsequent disease-targeted therapy research.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70075"},"PeriodicalIF":4.0,"publicationDate":"2026-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147929967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}