Cell Communication and Signaling最新文献

{"title":"A novel intracellular signaling pathway elicited by DM9CP-6 regulates immune responses in oysters.","authors":"Jiejie Sun, Yinan Li, Yu Liu, Lingling Wang, Linsheng Song","doi":"10.1186/s12964-025-02389-4","DOIUrl":"https://doi.org/10.1186/s12964-025-02389-4","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"383"},"PeriodicalIF":8.2,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979516","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":"Senescent fibroblasts secrete CTHRC1 to promote cancer stemness in hepatocellular carcinoma.","authors":"Hai Huang, Wang Peng, Qiaodan Zhou, Yuchong Zhao, Luyao Liu, Haochen Cui, Jingwen Liang, Mengdie Cao, Wei Chen, Ronghua Wang, Shiru Chen, Si Xiong, Bin Cheng, Shuya Bai","doi":"10.1186/s12964-025-02369-8","DOIUrl":"https://doi.org/10.1186/s12964-025-02369-8","url":null,"abstract":"<p><strong>Background: </strong>Cellular senescence plays a significant role in tumorigenesis and tumor progression. Substantial evidence indicates that senescence occurs in cancer-associated fibroblasts (CAFs), the predominant stromal component within the tumor microenvironment (TME), which profoundly impacts tumor biology. However, despite growing evidence of stromal cell involvement in cancer progression, the specific mechanisms and clinical implications of senescent CAFs (SCAFs) in hepatocellular carcinoma (HCC) have not been fully elucidated.</p><p><strong>Methods: </strong>The senescence signature was utilized to evaluate the senescence status of cell types within the TME of HCC using the GSE149614 dataset. The CytoTRACE and cell-cell communication analysis were used to find the correlation between cancer stemness and SCAFs. A risk prediction model associated with SCAFs was constructed to investigate potential mechanisms by which SCAFs promote tumor progression. Single-cell RNA sequencing data was used to identify senescent CAF-related genes. Gene expression and clinical data for HCC were obtained from the Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC), and National Omics Data Encyclopedia (NODE) databases. Using four machine-learning algorithms, crucial genes were identified to develop a CAF-senescence-related risk model, predicting prognosis, cancer stemness, immune infiltration, tumor mutation burden, and therapeutic responses in HCC patients. Next, we explored the role of Collagen Triple Helix Repeat Containing-1 (CTHRC1) in cancer stemness using both in vitro and in vivo experiments. Through various functional experiments, we elucidated the downstream signaling pathways of CTHRC1. Additionally, chromatin immunoprecipitation experiments were used to verify that key transcription factors bind to the CTHRC1 promoter region.</p><p><strong>Results: </strong>CAFs exhibited high senescence status and a strong correlation with cancer stemness in HCC. A novel CAF-senescence-score (CSscore) prognostic model was established for HCC based on 10 genes: CTHRC1, SERPINE1, RNF11, ENG, MARCKSL1, ASAP1, FHL3, LAMB1, CD151, and OLFML2B. The survival prediction performance was validated on TCGA, ICGC, and NODE cohorts. Immune analysis revealed that the CSscore was positively correlated with immunosuppressive immune cell populations, including M2 macrophages and regulatory T cells. Conversely, a negative correlation was observed between the CSscore and anti-tumor immune cells such as CD8 + T cells, dendritic cells, and B cells HCC patients with a low CSscore had a lower tumor mutation burden and showed improved responsiveness to immunotherapy and transarterial chemoembolization. In vitro experiments and bioinformatics analysis further revealed that CTHRC1 was significantly elevated in SCAFs promoted cancer stemness and metastasis via the SRY-box transcription factor 4 (SOX4)-CTHRC1-Notch1 axis in HCC.</p><p><strong>Conclusion: </","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"379"},"PeriodicalIF":8.2,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12376455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979566","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":"African swine fever virus A179L inhibits interferon induced transmembrane protein 1 activation of NF-κB pathway.","authors":"Xiamei Sun, Liqi Zhu, Chunxiao Mou, Jinyu Zhao, Yun Young Go, Kaichuang Shi, Zhenhai Chen","doi":"10.1186/s12964-025-02381-y","DOIUrl":"https://doi.org/10.1186/s12964-025-02381-y","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"380"},"PeriodicalIF":8.2,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12376476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979527","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":"Elevated levels of Letm1 drives mitochondrial dysfunction and cardiomyocyte stress-mediated apoptosis in cultured cardiomyocytes.","authors":"Anushka Deshpande, Leo Weirauch, Tapan Kumar Baral, Marco Steier, Ankush Borlepawar, Manju Kumari, Lucia S Kilian, Karsten Richter, Elke Hammer, Derk Frank, Constanze Schmidt, Norbert Frey, Ashraf Y Rangrez","doi":"10.1186/s12964-025-02378-7","DOIUrl":"https://doi.org/10.1186/s12964-025-02378-7","url":null,"abstract":"<p><strong>Background: </strong>Cardiac ischemia, a predominant cause of heart failure, is marked by profound mitochondrial dysfunction, dysregulated ion homeostasis, and maladaptive cellular remodeling, all of which compromise cardiac performance. The mitochondrial inner membrane protein Leucine zipper-EF-hand containing Transmembrane Protein 1 (Letm1), implicated in Wolf-Hirschhorn Syndrome, is essential for mitochondrial function. Although genetic alterations in Letm1 are linked to cardiomyopathies, its specific contributions to cardiac pathophysiology, particularly in the context of ischemic heart disease, remain poorly defined. This study aims to elucidate the role of Letm1 in ischemic cardiac pathology and its mechanistic impact on cardiomyocyte function.</p><p><strong>Methods: </strong>Letm1 expression was assessed in human and murine models of heart failure due to ischemic cardiomyopathy (ICM) and cardiac hypertrophy. Letm1 was overexpressed in neonatal rat ventricular cardiomyocytes, adult mouse cardiomyocytes, and human induced pluripotent stem cell (iPSC)-derived cardiomyocytes to study mitochondrial function (Seahorse assays), structural and molecular remodeling (fluorescence microscopy, transmission electron microscopy (TEM), qPCR, immunoblotting), transcriptomic/proteomic profiles, calcium handling and electrophysiology (patch-clamp), autophagic flux (Bafilomycin A1, LC3-RFP-GFP), and cell survival.</p><p><strong>Results: </strong>Letm1 was markedly upregulated in ICM in both human and murine hearts, but unchanged in hypertrophic heart failure. Overexpression of Letm1 in cardiomyocytes resulted in profound mitochondrial dysfunction, including downregulation of oxidative phosphorylation (OXPHOS) genes, impaired membrane potential, reduced ATP output, increased proton leak, and elevated ROS levels. A metabolic shift toward glycolysis was observed, accompanied by reduced fatty acid oxidation. Electron microscopy revealed mitochondrial fragmentation, mitophagic vesicles, and sarcomeric disarray. Transcriptomic and proteomic analyses highlighted dysregulation of genes linked to mitochondrial organization, ion transport, and autophagy. Electrophysiologically, Letm1 reduced L-type Ca<sup>2+</sup> current density and significantly shortened action potential duration, leading to impaired contractility. Letm1 overexpression activated upstream autophagy regulators (AMPK, ULK1) and enhanced LC3-II and p62 accumulation, but autophagic flux was impaired, as confirmed by LC3-RFP-GFP reporter and exacerbated by Bafilomycin A1 treatment. This dysregulated autophagy was coupled with mitochondrial stress, increased apoptosis (cleaved caspases), and reduced cardiomyocyte viability.</p><p><strong>Conclusion: </strong>This study indicates that Letm1 upregulation drives mitochondrial dysfunction, electrophysiology alterations, and activation of autophagy and apoptosis, culminating in cardiomyocyte injury in ischemic cardiomyopathy. By disrupting OXPHOS, c","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"378"},"PeriodicalIF":8.2,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979478","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":"MreB: unraveling the molecular mechanisms of bacterial shape, division, and environmental adaptation.","authors":"Yaqi Wang, Yalan Jiang, Zhixuan Song, Chengbin Zhu, Yujun Tang, Jiaofeng Peng, Peng Liu","doi":"10.1186/s12964-025-02373-y","DOIUrl":"https://doi.org/10.1186/s12964-025-02373-y","url":null,"abstract":"","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"377"},"PeriodicalIF":8.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12372405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979495","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":"Biomechanics of the tumor extracellular matrix and regulatory T cells: regulatory mechanisms and potential therapeutic targets.","authors":"Wen-Bo Huang, Heng-Zhou Lai, Jing Long, Zhuo-Ling Dai, Qiong Ma, Chong Xiao, Feng-Ming You","doi":"10.1186/s12964-025-02380-z","DOIUrl":"https://doi.org/10.1186/s12964-025-02380-z","url":null,"abstract":"<p><p>Tumor-infiltrating regulatory T cells (TI-Tregs) are characterized by their abnormal accumulation and heightened immunosuppressive activity. However, the biomechanical mechanisms that govern Treg identity and function through extracellular matrix (ECM) properties remain poorly understood. In three-dimensional culture systems and the tumor microenvironment (TME), increased matrix stiffness and viscoelasticity have been shown to promote Treg differentiation and expansion. Structural remodeling of the ECM, particularly the realignment of collagen fibers and the reduction in effective pore size, significantly enhances Treg migration. Moreover, biomechanical signals derived from the ECM strengthen the oxidative phosphorylation (OXPHOS) metabolic phenotype and immunosuppressive function of Tregs by modulating mitochondrial dynamics. This review provides a comprehensive analysis of the molecular events through which ECM mechanical properties-such as stiffness, viscoelasticity, and topological structure-regulate Treg identity and functionality, as well as the mechanical sensing and response mechanisms employed by Tregs. The potential for targeting Treg mechanosensors and mechanotransduction pathways to develop mechano-immunomodulatory strategies for cancer therapy is also discussed.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"375"},"PeriodicalIF":8.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979492","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":"Cisd2 delays atrial aging via a modulation of calcium homeostasis that mitigates atrial myopathy.","authors":"Chi-Hsiao Yeh, Zhao-Qing Shen, Li-Hsien Chen, Carol Seah, Tsai-Yu Tzeng, Chien-Yi Tung, Wen-Tai Chiu, Cheng-Heng Kao, Ting-Fen Tsai","doi":"10.1186/s12964-025-02377-8","DOIUrl":"https://doi.org/10.1186/s12964-025-02377-8","url":null,"abstract":"<p><p>Age-associated atrial myopathy results in structural remodeling and a disturbance of atrial conductance. Atrial myopathy often precedes atrial fibrillation (AF) and can facilitate AF progression. However, the molecular mechanism linking aging to atrial deterioration remains elusive. CDGSH iron-sulfur domain-containing protein 2 (CISD2) is a mammalian pro-longevity gene. We used Cisd2 knockout (Cisd2KO) and Cisd2 transgenic (Cisd2TG) mice to investigate pathophysiological mechanisms underlying age-related atrial myopathy. Four findings are pinpointed. Firstly, in both humans and mice, the level of atrial CISD2 declines during natural aging; this correlates with age-associated damage, namely degeneration of intercalated discs, mitochondria, sarcoplasmic reticulum (SR) and myofibrils. Secondly, in Cisd2KO and naturally aged wild-type mice, Cisd2 deficiency causes atrial electrical dysfunction and structural deterioration; conversely, sustained Cisd2 levels protect Cisd2TG mice against age-related atrial myopathy. Thirdly, Cisd2 plays a vital role in maintaining Ca²⁺ homeostasis in atrial cardiomyocytes. Cisd2 deficiency disrupts Ca²⁺ regulation, leading to elevated cytosolic Ca²⁺, reduced SR Ca²⁺, impaired store-operated calcium entry, and mitochondrial Ca²⁺ overload; these compromise mitochondrial function and attenuate antioxidant capability. Finally, transcriptomic analysis reveals that Cisd2 protects the atrium from metabolic reprogramming and preserves into old age a transcriptomic profile resembling a youthful pattern, thereby safeguarding the atrium from age-related injury. This study highlights Cisd2's crucial role in preventing atrial aging and underscores the therapeutic potential of targeting Cisd2 when combating age-associated atrial dysfunction, which may lead to the development of strategies for improving cardiac health in aging populations.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"376"},"PeriodicalIF":8.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979510","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":"The integrated stress response promotes macrophage inflammation and migration in autoimmune diabetes.","authors":"Jiayi E Wang, Charanya Muralidharan, Armando A Puente, Titli Nargis, Jacob R Enriquez, Ryan M Anderson, Raghavendra G Mirmira, Sarah A Tersey","doi":"10.1186/s12964-025-02372-z","DOIUrl":"10.1186/s12964-025-02372-z","url":null,"abstract":"<p><p>Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing pancreatic β-cells. Macrophages infiltrate islets early in T1D pathogenesis, preceding the influx of T- and B-lymphocytes. The integrated stress response (ISR), a cellular pathway activated during stress, coordinates adaptive changes in gene expression to maintain cell function and survival. To study the ISR in macrophages, bone-marrow-derived macrophages were treated with a pharmacological inhibitor of the ISR (ISRIB) and polarized to a proinflammatory M1-like state. We observed a reduction in the number of proinflammatory macrophages, as well as a decrease in iNOS mRNA and protein levels, following ISRIB treatment. RNA-sequencing revealed a reduction in pathways related to stress responses, including ER stress, reactive oxygen species (ROS) regulation, and autophagy, as well as migration pathway genes. ISRIB treatment led to decreased macrophage migration after stimulation in vitro and reduced migration of macrophages to the site of injury after tailfin injury in zebrafish in vivo. Interestingly, ISRIB mediated reduction of M1-like macrophages and reduction of migration was recapitulated by the inhibition of PKR but not PERK, both upstream ISR kinases, highlighting PKR as a key mediator of the ISR in macrophages. Pre-diabetic female non-obese diabetic (NOD) mice administered ISRIB demonstrated an overall reduction in the macrophage numbers in the pancreatic islets. Additionally, the insulitic area of pancreata from ISRIB treated NOD mice had increased PD-L1 levels. PD-L1 protein but not mRNA levels were increased in M1-like macrophages after ISR and PKR inhibition. Our findings identify the ISR, particularly via PKR, as a critical regulator of macrophage driven inflammation and migration in T1D. Our study offers new insights into ISR signaling in macrophages, demonstrating that the ISR may serve as a potential target for intervention in macrophages during early T1D pathogenesis.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"374"},"PeriodicalIF":8.2,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979590","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":"Immuno-metabolic diseases and therapeutics: molecular mechanisms via inflammasome signaling.","authors":"Joo-Hui Han","doi":"10.1186/s12964-025-02368-9","DOIUrl":"10.1186/s12964-025-02368-9","url":null,"abstract":"<p><p>Inflammatory responses serve as essential defense mechanisms in living organisms, but persistent or excessive activation can contribute to the development of chronic metabolic diseases. A central regulator of such inflammation is the inflammasome, a cytosolic multiprotein complex that senses pathogenic or stress-related signals and triggers the maturation of pro-inflammatory cytokines, particularly interleukin-1β (IL-1β) and interleukin-18 (IL-18). While inflammasome-induced pyroptosis, a form of lytic cell death, can play protective roles in pathogen clearance, excessive or dysregulated activation is more commonly associated with chronic inflammation and tissue damage. Increasing evidence points to the involvement of inflammasomes, especially the NLRP3 inflammasome, in the pathogenesis of immune-metabolic diseases that characterized by the interplay between immune dysfunction and metabolic imbalance, including obesity, diabetes, atherosclerosis, and sarcopenia. In these conditions, aberrant inflammasome activity contributes to insulin resistance, lipid dysregulation, muscle wasting, and vascular injury through sustained cytokine release and immune cell recruitment. Recent studies have advanced our understanding of how inflammasome signaling is integrated into the molecular landscape of metabolic disease, offering new insights into disease mechanisms and highlighting inflammasomes as viable therapeutic targets. This review provides an updated overview of inflammasome biology, defines their role in four representative immune-metabolic diseases, and discusses recent progress in targeting inflammasome pathways as a strategy to mitigate chronic inflammation and metabolic dysfunction.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"373"},"PeriodicalIF":8.2,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144884334","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":"Mild chronic stress promotes female fertility via the ovarian CRF receptor.","authors":"Eran Gershon, Orna Issler, Mariana Schroeder, Yael Kuperman, Nava Nevo, Shlomi Lazar, Michal Elbaz, Nava Dekel, Alon Chen","doi":"10.1186/s12964-025-02371-0","DOIUrl":"10.1186/s12964-025-02371-0","url":null,"abstract":"<p><strong>Background: </strong>In many species, including human, stress is accompanied by disruption of reproductive functions. The endocrine stress-response is activated and regulated by members of the corticotropin releasing factor (CRF) protein family. Stress stimuli may affect reproductive functions locally, recruiting autocrine/paracrine strategies. Yet, the molecular mechanisms mediating these effects are not fully understood.</p><p><strong>Methods: </strong>To explore the molecular mechanism mediating the ovarian stress response, we used three different models: (1) ICR mice subjected to chronic variable stress (CVS) procedure for 4 weeks. The stress procedure consisted of 9 different stressors per week, approximately 2 stressors per day both in the dark and the light phases. (2) wild-type mice undergoing intraovarian injection of the CRF receptor antagonist, β-asstressin, and (3) CRF-R1 knockout mice.</p><p><strong>Results: </strong>We report herein that ovulation rate was significantly elevated, and the litter size was substantially increased, in the following estrous cycle of female mice subjected to mild chronic variable stress (CVS). These females exhibited lower serum estrogen levels associated with reduced ovarian 17β-HSD3 expression. Exploration of the involvement of a neuroregulatory mechanism in this event revealed upregulation of the corticotropin releasing factor type 1 receptor (CRFR1) in the theca-interstitial cells of large ovarian follicles. In agreement, CRFR1 knockout mice, as well as wild-type females undergoing intraovarian injection of the CRF receptor antagonist, β-asstressin, displayed reduced ovulation rate, enhanced estrogen secretion and an increase in 17β-HSD3 expression.</p><p><strong>Conclusions: </strong>Our findings show a direct gonadal response to neuroendocrine and central stress-response regulators. The mechanism of this unexpected beneficial effect of CVS on reproduction may provide a neuro-endocrine background to the well-known \"Baby Boom\" phenomenon.</p>","PeriodicalId":55268,"journal":{"name":"Cell Communication and Signaling","volume":"23 1","pages":"372"},"PeriodicalIF":8.2,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144857102","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}