生理学报最新文献

{"title":"[Effects of interleukin-18 on CD4⁺PD-1⁺ T cells may contribute to the pathogenesis of immune thrombocytopenia].","authors":"Cen Yi, Cheng Zhang, Pei-Ning Li, Wei-Ping Li, Ying Zhou","doi":"10.13294/j.aps.2025.0084","DOIUrl":"10.13294/j.aps.2025.0084","url":null,"abstract":"<p><p>The aim of this study was to investigate the regulatory effect and mechanism of interleukin-18 (IL-18) on the function of human peripheral blood CD4⁺ programmed death-1 (PD-1)⁺ T cells , and to explore whether the role of IL-18 was involved in the pathogenesis of immune thrombocytopenia (ITP). Peripheral anticoagulant samples were collected from ITP patients and healthy control subjects, and peripheral blood mononuclear cells (PBMCs) from healthy controls were isolated. CD4⁺PD-1⁺ T cells were isolated by immunomagnetic bead method and used to establish T and B cells co-culture system. ELISA was used to detect the contents of IgG and IgM in cell culture supernatant. Flow cytometry was used to detect cytokine and co-stimulatory molecule expression levels. MitoSOX mitochondrial superoxide indicator was used to detect mitochondrial reactive oxygen species (ROS) levels. The results showed that, under IL-18 stimulation, the expression levels of CD40L and inducible co-stimulator (ICOS) on the surface of healthy control CD4⁺PD-1⁺ T cells were significantly up-regulated, and the abilities of these T cells to assist B cells in producing antibodies were significantly enhanced. IL-18 stimulation increased the mitochondrial ROS levels in healthy control CD4⁺PD-1⁺ T cells, promoting the secretion of interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α) by these T cells. This cytokine secretion promoting effect of IL-18 was inhibited by the ROS scavenger MitoQ. Compared to the healthy controls, the serum soluble PD-1 (sPD-1) level in the ITP patients was significantly increased. Under IL-18 stimulation, the sPD-1 level in the supernatant of healthy control CD4⁺ T cell culture was significantly increased. These results suggest that IL-18 may affect the function of CD4⁺PD-1⁺ T cells by regulating the production of mitochondrial ROS, and participate in their immune regulation through PD-1 pathway, thereby contributing to the pathogenesis of ITP.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"433-442"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research advances in the role of macrophages in the pathogenesis and treatment of sepsis-induced cardiomyopathy].","authors":"Xing-Min Ning, Zi-Kun Pei, Ren-Qi Li, Wei Peng, Jun Liang, Jia-Hui Zhu, Jian-Ming Pei, Jun Li","doi":"10.13294/j.aps.2026.0032","DOIUrl":"10.13294/j.aps.2026.0032","url":null,"abstract":"<p><p>Sepsis-induced cardiomyopathy (SIC) is a form of myocardial dysfunction induced by sepsis, which significantly increases mortality in septic patients. Its pathogenic mechanisms are highly complex, and there is currently no targeted treatment strategy. Macrophages (MΦ), as the most abundant immune cells in the heart, play an important role in the initiation, progression, and repair of SIC due to their high heterogeneity. Therefore, this review systematically summarizes the origin and function of cardiac MΦ and explores their potential pathways in the pathogenesis of SIC. Additionally, it highlights recent research advances in mitigating post-septic cardiac dysfunction and tissue damage by targeting the inhibition of inflammatory MΦ recruitment, specifically regulating MΦ inflammatory polarization and metabolic reprogramming, thus enhancing the activity of reparative MΦ. This review provides a theoretical basis for targeting MΦ in the prevention and treatment of SIC.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"385-394"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Advances in the roles and mechanisms of fibroblast growth factor family members in the self-renewal and differentiation of spermatogonial stem cells].","authors":"Guang-Hua Li, Ying Zheng","doi":"10.13294/j.aps.2026.0010","DOIUrl":"10.13294/j.aps.2026.0010","url":null,"abstract":"<p><p>The normal process of spermatogenesis constitutes the cornerstone of male fertility, wherein the maintenance and differentiation of spermatogonial stem cells (SSCs) are indispensable factors in regulating male fertility. Members of the fibroblast growth factor (FGF) family are requisite for the self-renewal and differentiation of SSCs. The core domain of FGF family members is composed of a conserved spherical or atypical β-trefoil structure, and these family members possess secretion function. These growth factors play a pivotal role in the development of organisms and in regulating cell proliferation, migration, and differentiation. Simultaneously, FGF family members regulate the process of self-renewal and differentiation of SSCs through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathways. This article reviews the latest research advancements in the regulation of SSCs' self-renewal and differentiation by members of the FGF family, with the expectation of deepening the understanding of key events in the development and maintenance of the male reproductive system, thereby providing novel ideas and theoretical bases for the diagnosis and treatment of infertility caused by male reproductive disorders.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"353-366"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The role and mechanism of autophagy regulator mTOR in renal ischemia-reperfusion injury].","authors":"Qian Luo, Shu-Han Yang, Xia Gong","doi":"10.13294/j.aps.2025.0106","DOIUrl":"10.13294/j.aps.2025.0106","url":null,"abstract":"<p><p>Renal ischemia-reperfusion injury (RIRI) is a major cause of acute kidney injury (AKI) and poor kidney transplantation outcomes. Its pathogenesis is closely related to oxidative stress, autophagy, and endoplasmic reticulum stress, although the specific mechanism is still unclear. The mammalian target of rapamycin (mTOR), as a key regulator of autophagy, plays critical roles at various stages of RIRI through different signaling pathways and contributes to mitigating renal damage. However, the underlying mechanisms require further studies. This review focuses on the role and mechanism of mTOR in RIRI and discusses the potential of mTOR as a therapeutic target.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"375-384"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The roles and regulatory mechanisms of serum and glucocorticoid-regulated kinase 1 in miscarriage and preeclampsia].","authors":"Chen Ye, Qing-Shen Wu, Xiao-Xuan Sun, Xiao-Qing Zhang, Lu Gao","doi":"10.13294/j.aps.2026.0028","DOIUrl":"10.13294/j.aps.2026.0028","url":null,"abstract":"<p><p>Serum and glucocorticoid-regulated kinase 1 (SGK1) is a serine/threonine kinase belonging to the AGC kinase family. SGK1 is widely expressed in diverse tissues, whose expression and activity are regulated by numerous physiological and pathophysiological factors, including glucocorticoids, mineralocorticoids, dehydration, ischemia, hyperosmotic stress, and radiation therapy. Following activation of the phosphatidylinositide 3-kinase (PI3K) signaling pathway, SGK1 is phosphorylated at its hydrophobic motif by the mechanistic target of rapamycin complex 2 (mTORC2) and at its kinase domain by 3-phosphoinositide-dependent protein kinase-1 (PDK1), thereby inducing its activation. Activated SGK1 subsequently upregulates the expression of various ion channels, such as Na⁺, Ca²⁺, K⁺, and Cl^- channels. Furthermore, SGK1 participates in regulating the expression and activity of multiple transcription factors (e.g., FKHRL1/FOXO3a, β-catenin, NF-κB, and p53), thereby influencing fundamental cellular processes including proliferation, survival, apoptosis, substance transport, glycolysis, and angiogenesis. Consequently, dysregulation of SGK1 expression or activity is implicated in the pathogenesis of various diseases, including hypertension, cancer, autoimmune disorders, and neurodegenerative diseases. Of particular note, SGK1 exhibits high expression in the human endometrial epithelium and is involved in the regulation of multiple aspects of pregnancy. This review summarizes the role of SGK1 in the pathogenesis of spontaneous abortion and preeclampsia, with a focus on its regulatory mechanisms involving the epithelial sodium channel (ENaC), the NF-κB signaling pathway, trophoblast cell apoptosis, and maternal-fetal blood vessel formation. We also prospect the potential of SGK1 as a therapeutic target for pregnancy-related disorders by modulating immune cell functions.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"367-374"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Progress on the mechanism of endocannabinoids involved in electroacupuncture for analgesia and itch relief].","authors":"Yu-Wei Cao, Ren-Jie Qin, Xiang-Hong Jing, Zhao-Qing Zhang, Man Li","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic pain and pruritus are significant health challenges that pose major threats to human well-being, with existing therapeutic approaches being limited in their efficacy and scope. Electroacupuncture, as a therapy developed by combining traditional acupuncture with modern electrophysiological techniques, has emerged as a promising therapeutic modality, characterized by its low risk and excellent tolerability, and has demonstrated unique advantages in the treatment of related disorders. In recent years, the role of the endocannabinoid system in modulating pain and pruritus has garnered increasing attention as a research hotspot. This review systematically examined the composition and function of the endocannabinoid system, as well as its regulatory mechanisms in pain and pruritus signaling within the central nervous system and peripheral immune system. Additionally, we summarized the current state of research on the analgesic and itch-relieving effects of electroacupuncture through modulation of the endocannabinoid system, aiming to provide novel insights and theoretical foundations for the clinical management of pain and itch-related diseases.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"71-82"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Differential effects of GluN2A and GluN2B subunits in the medial prefrontal cortex on chronic pain and anxiety/depressive-like behaviors].","authors":"Jia-Li Ding, Hui-Ran Yang, Yu-Qiu Zhang, Hong Cao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This study aimed to investigate the differential roles of GluN2A and GluN2B subunits of <i>N</i>-methyl-<i>D</i>-aspartate receptor (NMDAR) in the medial prefrontal cortex (mPFC) and their downstream signaling pathways in a mouse model of chronic constrictive injury of the infraorbital nerve (CION)-induced pain and anxiety/depression-like behaviors. A mouse model of trigeminal neuropathic pain was established under CION surgery. Behavioral tests were conducted to assess mechanical thresholds and anxiety/depression-like behaviors. The protein expression levels of GluN2A, GluN2B, ERK and mTOR in the mPFC were detected by Western blot. GluN2A antagonist (PEAQX) and GluN2B antagonist (Ifenprodil) were microinjected into the mPFC to observe their behavioral effects and underlying molecular mechanisms. CION mice developed persistent pain and anxiety/depression-like behaviors, accompanied by increased GluN2B expression in the mPFC. Behavioral results showed that compared with the vehicle group, GluN2A antagonist PEAQX ameliorated anxiety/depression-like behaviors, but not pain hyperalgesia. However, GluN2B antagonist Ifenprodil significantly alleviated pain and depressive-like symptoms instead of anxiety-like behaviors. Western blot analysis revealed that PEAQX significantly increased the expression of phosphorylation of ERK1 and ERK2, while reduced the expression of both total ERK1 and total ERK2. On the other hand, Ifenprodil decreased the expression of total mTOR protein. Neither antagonist had a significant effect on phospho-mTOR levels. Taken together, our findings suggest that GluN2A and GluN2B subunits in the mPFC differentially contribute to chronic pain and anxiety/depressive-like behaviors through their respective intracellular signaling. This study provides novel insights into the mechanisms underlying chronic pain and emotional comorbidity, and offers experimental evidence for developing targeted therapeutic strategies against specific NMDAR subunits.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"195-206"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on mitochondrial genetic mechanisms underlying the onset of migraine].","authors":"Meng-Yuan Qiu, Huai-Lian Guo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Migraine is a common primary headache disorder in clinical practice, and its recurrent nature severely impairs patients' quality of life. Data from the 2021 Global Burden of Disease Study indicate that migraine imposes a heavy burden on patients, their families, and society. In recent years, the association between mitochondrial dysfunction and migraine has attracted increasing attention. Studies have demonstrated that during migraine attacks, skeletal muscle cells exhibit significant mitochondrial morphological changes (such as mitochondrial swelling and cristae disruption), while platelets show mitochondrial biochemical abnormalities (e.g., reduced respiratory chain enzyme activity). Impaired energy metabolism in the brain tissue of migraine patients suggests that mitochondrial dysfunction may be involved in the pathogenesis of migraine. With rapid advances in technologies such as high-throughput sequencing and targeted sequencing, genetic variations in mitochondrial DNA (mtDNA) have gradually become a research hotspot in the etiology of migraine. Several studies have identified mtDNA genetic variations in migraine patients, which may affect the onset and progression of migraine by regulating mitochondrial energy metabolism pathways and inducing oxidative stress. This article systematically summarizes recent research progress on the correlation between migraine and mtDNA, focuses on classifying the main types and characteristics of mtDNA variations, analyzes the controversies and limitations of current studies, and outlines future research directions, thereby providing an important reference for exploring the etiology of migraine.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"101-108"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mice with postsurgical pain exhibit age-dependent spinal microglial activation and inhibitory synapse loss.","authors":"Jia-Ning Wang, Yu Shen, Shi-Hao Wang, Ping Liao, Ruo-Tian Jiang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Persistent postsurgical pain is a major clinical concern, especially in the aging population, who represent a growing proportion of surgical patients. Although age is a known pain risk factor, the mechanisms driving age-related vulnerability to chronic postoperative pain remain poorly understood. This study aims to investigate how aging influences the resolution of postoperative pain and to elucidate the roles of microglial activation and synaptic remodeling in the spinal dorsal horn. A plantar incision model in young (3-month-old) and aged (18-month-old) male and female mice was used to mimic postoperative pain conditions. Mechanical and thermal hypersensitivity at various postoperative intervals were assessed by von Frey and Hargreaves tests. Microglial activation and inhibitory/excitatory synaptic densities in the spinal dorsal horn were evaluated using immunofluorescence and 3D reconstruction with Imaris software. On postoperative day (POD) 3, both age groups exhibited reduced pain thresholds on the ipsilateral side, along with microglial activation in the dorsal horn. On POD 7, pain thresholds in young mice had returned to baseline with no significant microglial activation, while aged mice showed sustained reduction in pain thresholds, continuous microglial activation, and significant loss of inhibitory synapses without detectable changes in excitatory synapse density. These findings are consistent across both sexes, with no sex-related differences. Collectively, these results suggest that aging is associated with persistent postoperative pain, which correlates with microglial activation and inhibitory synapse loss. These insights advance our understanding of age-related pain vulnerability and may inform the development of more effective, targeted, and age-specific therapeutic strategies to prevent or alleviate persistent postoperative pain in elderly patients.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"182-194"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanistic insights into NLRP3 inflammasome regulation of chronic pain].","authors":"Zong-Zhi Yang, Jie Wu, Xiao-Lan Huang, Dong-Lin Xiong, Yu-Hui Luo, Li-Zu Xiao, Bi-Fa Fan, Chang-Yu Jiang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The NLRP3 inflammasome, a pivotal effector of the innate immune system, has emerged as a critical regulator in the initiation and maintenance of chronic pain. Accumulating evidence demonstrates that NLRP3 inflammasome activation in the peripheral nervous system, particularly in dorsal root ganglia (DRG), promotes the release of pro-inflammatory mediators such as interleukin-1β (IL-1β), enhances sensory neuronal excitability, and facilitates nociceptive signal transmission and amplification. Moreover, satellite glial cells and infiltrating immune cells within the DRG contribute to the establishment of an inflammatory microenvironment, forming a neuron-glia-immune network that drives pain sensitization. In the central nervous system, activation of the NLRP3 inflammasome in microglia and astrocytes induces alterations in synaptic plasticity and central sensitization, further exacerbating the aberrant amplification of pain signals. This review summarizes recent advances in elucidating the regulatory mechanisms of the NLRP3 inflammasome in chronic pain in both peripheral and central nervous systems, providing a theoretical foundation for the development of novel analgesic strategies targeting the inflammasome.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"135-147"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}