生理学报最新文献

{"title":"[Steroid sulfatase inhibitor DU-14 prevents amyloid β-protein-induced depressive-like behavior and theta rhythm suppression in rats].","authors":"Xing-Hua Yue, Zhao-Jun Wang, Mei-Na Wu, Hong-Yan Cai, Jun Zhang","doi":"10.13294/j.aps.2025.0052","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0052","url":null,"abstract":"<p><p>The hippocampus, a major component of the limbic system, is the most important region related to emotion regulation and memory processing. Cognitive impairment and depressive symptoms observed in Alzheimer's disease (AD) patients may be attributed to hippocampal damage caused by amyloid β-protein (Aβ). Our previous studies have demonstrated that a steroid sulfatase inhibitor DU-14 can enhance hippocampal synaptic plasticity and spatial memory abilities in a chronic AD murine model by counteracting the toxic effects of Aβ. However, limited experimental evidence exists regarding the efficacy of steroid sulfatase inhibitor on depressive symptoms in AD animal models. In this study, we investigated the effects of DU-14 on depressive symptoms and theta-band neuronal oscillations in rats with intrahippocampal injection of Aβ_1-42 using various behavioral tests such as sucrose preference test, tail suspension test, forced swimming test, and <i>in vivo</i> hippocampal local field potential (LFP) recording. The results demonstrated that, in comparison to the control group: (1) rats in the Aβ group exhibited a decrease in sucrose preference, indicating a loss of interest in pleasurable activities; (2) rats in the Aβ group displayed aggravated depressive-like behavior characterized by prolonged immobility time during tail suspension and forced swimming tests; (3) Aβ disrupted the induction of theta rhythm via tail pinch stimulation, and resulted in a significant reduction in peak power of theta rhythm. In contrast to the Aβ group, pretreatment with DU-14 resulted in: (1) a significant improvement in Aβ-induced anhedonia, as evidenced by increased sucrose preference; (2) significant alleviation of Aβ-induced despair and depressive-like behaviors, reflected by reduced immobility time during tail suspension and forced swimming tests; (3) successful mitigation of Aβ-mediated inhibition on bilateral hippocampal theta rhythm. These findings indicate that steroid sulfatase inhibitor DU-14 can counteract neurotoxicity induced by Aβ, and prevent Aβ-induced depressive-like behavior and suppression of theta rhythm.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"801-810"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407724","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":"Targeting WEE1: a rising therapeutic strategy for hematologic malignancies.","authors":"Hao-Bo Li, Thekra Khushafa, Chao-Ying Yang, Li-Ming Zhu, Xing Sun, Ling Nie, Jing Liu","doi":"10.13294/j.aps.2025.0058","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0058","url":null,"abstract":"<p><p>Hematologic malignancies, including leukemia, lymphoma, and multiple myeloma, are hazardous diseases characterized by the uncontrolled proliferation of cancer cells. Dysregulated cell cycle resulting from genetic and epigenetic abnormalities constitutes one of the central events. Importantly, cyclin-dependent kinases (CDKs), complexed with their functional partner cyclins, play dominating roles in cell cycle control. Yet, efforts in translating CDK inhibitors into clinical benefits have demonstrated disappointing outcomes. Recently, mounting evidence highlights the emerging significance of WEE1 G2 checkpoint kinase (WEE1) to modulate CDK activity, and correspondingly, a variety of therapeutic inhibitors have been developed to achieve clinical benefits. Thus, WEE1 may become a promising target to modulate the abnormal cell cycle. However, its function in hematologic diseases remains poorly elucidated. In this review, focusing on hematologic malignancies, we describe the biological structure of WEE1, emphasize the latest reported function of WEE1 in the carcinogenesis, progression, as well as prognosis, and finally summarize the therapeutic strategies by targeting WEE1.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"839-854"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407765","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":"[Glutamatergic neurons in thalamic paraventricular nucleus may be involved in the regulation of abnormal sleep behavior of <i>Shank3</i> gene knockout mice].","authors":"Chang-Feng Chen, Lie-Cheng Wang, Yong Liu, Lei Chen","doi":"10.13294/j.aps.2025.0041","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0041","url":null,"abstract":"<p><p>The purpose of this study was to investigate the anxiety-like behaviors, circadian rhythms and sleep, and to elucidate the possible underlying mechanisms of the abnormal sleep behavior in <i>Shank3</i> gene knockout (<i>Shank3</i>-KO) mice. The anxiety-like behaviors were detected by elevated plus-maze (EPM) test, open field test (OFT) and tail suspension test (TST). The circadian rhythms were detected by running wheel test. The electroencephalogram (EEG)/electromyogram (EMG) recordings were performed synchronically by polysomnograph. The distribution of SHANK3 in anterior cingulate cortex (ACC), paraventricular thalamus (PVT), nucleus accumbens (NAc), basolateral amygdala (BLA) and hippocampal CA2 region in wild type (WT) mice was detected by immunofluorescence assay. The protein expression of c-Fos in PVT, ACC and NAc was also detected by immunofluorescence assay during light cycle. The colocalization of c-Fos and vesicular glutamate transporter 2 (Vglut2, a marker for glutamatergic neurons) in the PVT was detected by immunofluorescence double labeling experiment. The results of EPM test showed that, compared with the WT mice, the <i>Shank3</i>-KO mice showed less time in open arms and less number of open arm entries. The results of OFT showed that the <i>Shank3</i>-KO mice showed less time in central area and less number of central area entries. The immobility time of <i>Shank3</i>-KO mice was increased in the TST. The results of running wheel rhythm test showed that the phase shift time of <i>Shank3</i>-KO mice in the continuous dark period was increased. The results of EEG/EMG recording showed that, compared with the WT mice, the duration of wakefulness in <i>Shank3</i>-KO mice was increased and the duration of non-rapid eye movement (NREM) sleep was decreased during light phase; The bout number of wakefulness was increased, the bout number of NREM sleep was decreased, NREM-wake transitions were increased, and wake-NREM transitions were decreased during light phase. SHANK3 was expressed in ACC, PVT, NAc and BLA in the WT mice. The expression of c-Fos in the PVT of <i>Shank3</i>-KO mice was up-regulated 2 h after entering the light phase, and majority of c-Fos was co-localized with Vglut2. These results suggest that the anxiety level of <i>Shank3</i>-KO mice is increased, the regulation of the internal rhythms is decreased, and the bout number of wakefulness is increased during light phase. The glutamatergic neurons in PVT may be involved in the regulation of abnormal sleep behavior in <i>Shank3</i>-KO mice during the light phase.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"792-800"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407555","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 MAP1 family: a new perspective for exploring unknown functions].","authors":"Qing Wang, Mei Liu, Zhang-Ji Dong","doi":"10.13294/j.aps.2025.0062","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0062","url":null,"abstract":"<p><p>As an important part of the cytoskeleton, microtubules play a crucial role in many cellular processes, such as cell division, intracellular transport, and maintaining cell morphology. The MAP1 family is an important family of microtubule-associated proteins, which includes three members: MAP1A, MAP1B, and MAP1S. These proteins are widely involved in the dynamic regulation of the cytoskeleton and play a key role in the development and function of the central nervous system, especially in the development and function of neurons. This study reviews the research progress of the MAP1 family, mainly focusing on the structure and function of MAP1 family members, and paying particular attention to their roles in neuronal development and regeneration, regulatory mechanisms, and neurodegenerative diseases.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"876-892"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407676","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 the protective effects of heat acclimation on the cardiova-scular system and its molecular mechanisms].","authors":"Guo-Yu Li, Feng Guo, Zhuo Wang, Yue Huang","doi":"10.13294/j.aps.2025.0050","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0050","url":null,"abstract":"<p><p>Heat acclimation provides cardiovascular protection in high-temperature environments through multilevel mechanisms; however, the complete molecular basis of its effects remains unclear. In this paper, we systematically review the effects of heat acclimation on blood volume, vascular function, cardiac structure, energy metabolism, and anti-stress regulation, revealing their potential mechanisms in cardiovascular adaptive protection. We also summarizes the multilevel responses induced by heat stress and heat acclimation, including the modulatory effects of heat acclimation on heat shock proteins (HSPs), hypoxia inducible factor 1 (HIF-1), and apoptotic pathways. Additionally, we highlights the comprehensive protective effects of heat acclimation across various stressors (e.g., hypoxia, heat stress). This review provides a significant physiological basis for cardiovascular disease management and sports medicine, emphasizing the potential application of heat acclimation in response to multiple stressors and supporting its role as an effective tool in cardiovascular health management and stress protection interventions.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"820-838"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407702","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":"[Molecular mechanism of transcription factor PU.1 regulating erythroid differentiation and its role in hematological diseases].","authors":"Zi-Jiang Yang, Dan Hu, Xiu-Juan Zhang","doi":"10.13294/j.aps.2025.0076","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0076","url":null,"abstract":"<p><p>Transcription factor PU.1, as a core member of the ETS family, plays a pivotal role in the multi-lineage differentiation of hematopoietic stem cells, particularly in the regulation of erythroid differentiation. PU.1 orchestrates the process of hematopoietic stem cell differentiation towards erythroid cells by modulating the transcription of lineage-determining factors and interacting with other key transcription factors in a fine-tuned manner. PU.1 plays an irreplaceable role in the development and function of red blood cells, with its abnormal expression closely related to the occurrence and progression of various blood diseases, including leukemia, myelodysplastic syndromes, and various types of anemia. This article comprehensively analyzes the functional roles and molecular mechanisms of PU.1 in various stages of erythroid differentiation, as well as its potential roles in related blood diseases. This review not only deepens our understanding of the mechanism by which PU.1 regulates erythroid differentiation, but also provides theoretical grounds for blood disease therapies based on PU.1.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"855-866"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407550","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":"[Multi-organ inflammatory phenotypes and transcriptomic characterization in an inflammation-driven mouse model of preeclampsia induced by LPS].","authors":"Ning Wang, Jing-Qiu Feng, Ying Xie, Meng-Can Sun, Qi Wang, Zhe Wang, Lu Gao","doi":"10.13294/j.aps.2025.0042","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0042","url":null,"abstract":"<p><p>Preeclampsia (PE) is a severe gestational disorder characterized by hypertension and proteinuria, with a subset of cases exhibiting an immune-driven phenotype marked by placental overexpression of proinflammatory cytokines and chronic inflammatory damage, profoundly impacting fetal development. To elucidate the pathophysiology of this PE subtype, we established an inflammation-driven PE mouse model via lipopolysaccharide (LPS) intraperitoneal injection, systematically evaluating histopathological changes in maternal heart, liver, lung, kidney, and placenta, and integrating transcriptomic profiling to uncover molecular mechanisms. LPS administration robustly induced maternal hypertension and proteinuria, hallmarks of PE, without significantly altering organ or fetal weights. Histological analyses revealed pronounced inflammatory damage in the maternal lung, kidney, and placenta, with the lung exhibiting the most severe pathology, characterized by inflammatory cell infiltration, alveolar wall thickening, and interstitial edema-challenging the conventional focus on placental and renal primacy in PE. Placental labyrinth and junctional zones displayed extensive structural disruption and necrosis, indicating functional impairment. Transcriptomic analysis identified 27 inflammation-related genes consistently upregulated across tissues, with protein-protein interaction networks pinpointing <i>Il1β</i>, <i>Il6</i>, <i>Ccl5</i>, <i>Ccl2</i>, <i>Cxcl10</i>, <i>Tlr2</i>, and <i>Icam1</i> as hub genes. Quantitative PCR validation confirmed <i>Tlr2</i> as a central regulator, evidenced by significant upregulation of <i>Tlr2</i> in lung, kidney, and placenta of LPS-induced PE mice, while <i>Cxcl10</i> exhibited placenta-specific upregulation, suggesting a synergistic inflammatory axis in placental pathology. These findings highlight the lung as a critical, yet underappreciated, target in inflammation-driven PE, reframe the multi-organ inflammatory landscape of the disease, and nominate <i>Tlr2</i> and <i>Cxcl10</i> as potential diagnostic biomarkers and therapeutic targets, offering new avenues for precision intervention in PE.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"775-791"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407602","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":"Conserved translational control in cardiac hypertrophy revealed by ribosome profiling.","authors":"Bao-Sen Wang, Jian Lyu, Hong-Chao Zhan, Yu Fang, Qiu-Xiao Guo, Jun-Mei Wang, Jia-Jie Li, An-Qi Xu, Xiao Ma, Ning-Ning Guo, Hong Li, Zhi-Hua Wang","doi":"10.13294/j.aps.2025.0077","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0077","url":null,"abstract":"<p><p>A primary hallmark of pathological cardiac hypertrophy is excess protein synthesis due to enhanced translational activity. However, regulatory mechanisms at the translational level under cardiac stress remain poorly understood. Here we examined the translational regulations in a mouse cardiac hypertrophy model induced by transaortic constriction (TAC) and explored the conservative networks <i>versus</i> the translatome pattern in human dilated cardiomyopathy (DCM). The results showed that the heart weight to body weight ratio was significantly elevated, and the ejection fraction and fractional shortening significantly decreased 8 weeks after TAC. Puromycin incorporation assay showed that TAC significantly increased protein synthesis rate in the left ventricle. RNA-seq revealed 1,632 differentially expressed genes showing functional enrichment in pathways including extracellular matrix remodeling, metabolic processes, and signaling cascades associated with pathological cardiomyocyte growth. When combined with ribosome profiling analysis, we revealed that translation efficiency (TE) of 1,495 genes was enhanced, while the TE of 933 genes was inhibited following TAC. In DCM patients, 1,354 genes were upregulated <i>versus</i> 1,213 genes were downregulated at the translation level. Although the majority of the genes were not shared between mouse and human, we identified 93 genes, including <i>Nos3</i>, <i>Kcnj8</i>, <i>Adcy4</i>, <i>Itpr1</i>, <i>Fasn</i>, <i>Scd1</i>, etc., with highly conserved translational regulations. These genes were remarkably associated with myocardial function, signal transduction, and energy metabolism, particularly related to cGMP-PKG signaling and fatty acid metabolism. Motif analysis revealed enriched regulatory elements in the 5' untranslated regions (5'UTRs) of transcripts with differential TE, which exhibited strong cross-species sequence conservation. Our study revealed novel regulatory mechanisms at the translational level in cardiac hypertrophy and identified conserved translation-sensitive targets with potential applications to treat cardiac hypertrophy and heart failure in the clinic.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"757-774"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407671","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 the comorbidity mechanism of sarcopenia and obesity in the aging population].","authors":"Hao-Dong Tian, Yu-Kun Lu, Li Huang, Hao-Wei Liu, Hang-Lin Yu, Jin-Long Wu, Han-Sen Li, Li Peng","doi":"10.13294/j.aps.2025.0079","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0079","url":null,"abstract":"<p><p>The increasing prevalence of aging has led to a rising incidence of comorbidity of sarcopenia and obesity, posing significant burdens on socioeconomic and public health. Current research has systematically explored the pathogenesis of each condition; however, the mechanisms underlying their comorbidity remain unclear. This study reviews the current literature on sarcopenia and obesity in the aging population, focusing on their shared biological mechanisms, which include loss of autophagy, abnormal macrophage function, mitochondrial dysfunction, and reduced sex hormone secretion. It also identifies metabolic mechanisms such as insulin resistance, vitamin D metabolism abnormalities, dysregulation of iron metabolism, decreased levels of nicotinamide adenine dinucleotide, and gut microbiota imbalances. Additionally, this study also explores the important role of genetic factors, such as alleles and microRNAs, in the co-occurrence of sarcopenia and obesity. A better understanding of these mechanisms is vital for developing clinical interventions and preventive strategies.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"905-924"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407660","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 of selenoproteins in adipose tissue and obesity].","authors":"Yun-Fei Zhao, Yu-Hang Sun, Tai-Hua Jin, Yue Liu, Yang-Di Chen, Wan Xu, Qian Gao","doi":"10.13294/j.aps.2025.0082","DOIUrl":"https://doi.org/10.13294/j.aps.2025.0082","url":null,"abstract":"<p><p>Selenoproteins, as the active form of selenium, play an important role in various physiological and pathological processes, such as anti-oxidation, anti-tumor, immune response, metabolic regulation, reproduction and aging. Although the expression level of selenoproteins in adipose tissue is significantly influenced by dietary selenium intake, it is closely related to the homeostasis of adipose tissue. In this review, we summarized the role of selenoproteins in the physiological function of adipose tissue and the pathogenesis of obesity in recent years, in order to provide a rationale for developing potential therapeutic agents for the treatment of obesity and related metabolic diseases.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"77 5","pages":"939-955"},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407711","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}