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LAMC1 aggravates diabetic retinopathy through PI3K/AKT signaling-regulated epithelial-mesenchymal transition in retinal pigment epithelial cells. LAMC1通过PI3K/AKT信号调节视网膜色素上皮细胞的上皮-间质转化,加重糖尿病视网膜病变。
IF 3.2 4区 医学
Journal of Physiological Sciences Pub Date : 2025-10-01 DOI: 10.1016/j.jphyss.2025.100045
Lei Liu, Yanlin Gao, Shiqi Yao
{"title":"LAMC1 aggravates diabetic retinopathy through PI3K/AKT signaling-regulated epithelial-mesenchymal transition in retinal pigment epithelial cells.","authors":"Lei Liu, Yanlin Gao, Shiqi Yao","doi":"10.1016/j.jphyss.2025.100045","DOIUrl":"https://doi.org/10.1016/j.jphyss.2025.100045","url":null,"abstract":"<p><p>Diabetic retinopathy (DR), a leading cause of adult blindness, with LAMC1-mediated epithelial-mesenchymal transition (EMT) playing a key role. By analyzing DR-related microarray datasets (GSE60436/GSE102485) from GEO, we identified 685 differentially expressed genes (570 downregulated, 115 upregulated). Functional and WGCNA analyses linked these to PI3K/Akt signaling, revealing 11 diagnostic hub genes, including LAMC1. Western blot analysis confirmed that LAMC1 significantly upregulated in high glucose (HG)-treated ARPE-19 cells and diabetic mouse retinas. In vitro and in vivo experiments confirmed that LAMC1 promotes EMT in retinal pigment epithelial (RPE) cells via PI3K/Akt activation, enhancing migration and invasion. Conversely, LAMC1 knockdown alleviated retinal damage in diabetic mice. Our studies uncovered that LAMC1's role in DR progression through PI3K/Akt-driven EMT, suggesting its potential as a therapeutic target.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 3","pages":"100045"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145301680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Estradiol enhances thermoregulation induced by ostruthin, a TREK channel agonist, in ovariectomized rats. 雌二醇增强去卵巢大鼠由卵磷脂(一种TREK通道激动剂)诱导的体温调节。
IF 3.2 4区 医学
Journal of Physiological Sciences Pub Date : 2025-09-26 DOI: 10.1016/j.jphyss.2025.100044
Yuki Uchida, Shotaro Kamijo, Yuki Samejima, Hiroshi Onimaru, Masahiro Hosonuma, Hikaru Isobe, Keiko Ikeda, Motoyasu Honma, Yuri Masaoka, Masahiko Izumizaki
{"title":"Estradiol enhances thermoregulation induced by ostruthin, a TREK channel agonist, in ovariectomized rats.","authors":"Yuki Uchida, Shotaro Kamijo, Yuki Samejima, Hiroshi Onimaru, Masahiro Hosonuma, Hikaru Isobe, Keiko Ikeda, Motoyasu Honma, Yuri Masaoka, Masahiko Izumizaki","doi":"10.1016/j.jphyss.2025.100044","DOIUrl":"10.1016/j.jphyss.2025.100044","url":null,"abstract":"<p><p>Menopausal women frequently report contradictory thermoregulatory symptoms (hot flashes and chills), believed to result from declining estradiol (E₂) levels; however, mechanisms remain unclear. TWIK-related (TREK) potassium channels function as cold receptors. Although E₂ enhances TREK1 activity in vitro, its effect on TREK-mediated thermoregulation has not been investigated in vivo. This study investigated whether E₂ facilitated TREK-mediated thermoregulation in ovariectomized rats using ostruthin, a TREK agonist. Rats were ovariectomized and implanted with silastic tubes with or without E₂, followed by ostruthin or vehicle injection. We measured thermoregulatory parameters, plasma hormones (triiodothyronine and thyroxine), and mRNA expression of cold receptors in dorsal root ganglia. Ventral root responses were examined in vitro. Ostruthin increased body temperature in E₂(+) versus E₂(-) groups, with increased triiodothyronine and upregulation of Trek1, Vgf, and Nos1. Ostruthin enhanced ventral root responses. These findings demonstrate that E₂ potentiates TREK-mediated thermoregulation through enhanced cold sensing, providing insights into menopausal disorders.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 3","pages":"100044"},"PeriodicalIF":3.2,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12509895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Incompleteness of the circle of Willis affects sleep quality, cognitive function and inflammation in patients with primary hypertension. 威利斯肌圈不完整影响原发性高血压患者的睡眠质量、认知功能和炎症。
IF 3.2 4区 医学
Journal of Physiological Sciences Pub Date : 2025-08-28 DOI: 10.1016/j.jphyss.2025.100043
Ying Feng, Xueqi Yang, Yang Song, Yu Zhang, Tianning Zhang, Chenglong Yu
{"title":"Incompleteness of the circle of Willis affects sleep quality, cognitive function and inflammation in patients with primary hypertension.","authors":"Ying Feng, Xueqi Yang, Yang Song, Yu Zhang, Tianning Zhang, Chenglong Yu","doi":"10.1016/j.jphyss.2025.100043","DOIUrl":"10.1016/j.jphyss.2025.100043","url":null,"abstract":"<p><p>To investigate whether incomplete Circle of Willis (Incomplete CoW) affects neuropsychological outcomes in patients with primary hypertension, a cross-sectional study was conducted involving 150 patients diagnosed with primary hypertension, a population at increased risk for neurovascular compromise. Magnetic Resonance Angiography was used to classify patients into two groups: Complete CoW (n = 41) and Incomplete CoW (n = 85). Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), and cognitive function was evaluated using the Mini-Mental State Examination (MMSE). PSQI scores were significantly higher in the Incomplete CoW group compared to the Complete CoW group, indicating poorer sleep quality in patients with an Incomplete CoW. A significant negative correlation was found between PSQI and MMSE scores in the Incomplete CoW group, linking poor sleep quality with cognitive impairment. These findings suggest that the incompleteness of the CoW may contribute to neuropsychological impairments in patients with hypertension, potentially mediated by enhanced inflammatory responses. DATA AVAILABILITY: The data used to support the findings of this study are available from the corresponding author upon request.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 3","pages":"100043"},"PeriodicalIF":3.2,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ATF4 transcriptionally activates NUPR1 to promote ferroptosis in chondrocytes and osteoarthritis development. ATF4转录激活NUPR1,促进软骨细胞铁下垂和骨关节炎的发展。
IF 3.2 4区 医学
Journal of Physiological Sciences Pub Date : 2025-08-05 DOI: 10.1016/j.jphyss.2025.100039
Chen Kuang, Taiyang Liao, Lishi Jie, Yibao Wei, Deren Liu, Enrui Hu, Liang Ding, Peimin Wang
{"title":"ATF4 transcriptionally activates NUPR1 to promote ferroptosis in chondrocytes and osteoarthritis development.","authors":"Chen Kuang, Taiyang Liao, Lishi Jie, Yibao Wei, Deren Liu, Enrui Hu, Liang Ding, Peimin Wang","doi":"10.1016/j.jphyss.2025.100039","DOIUrl":"10.1016/j.jphyss.2025.100039","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a common degenerative joint disease characterized by cartilage destruction and inflammation. This study reveals that activating transcription factor 4 (ATF4) is upregulated in IL-1β-treated chondrocytes and promotes ferroptosis, a form of programmed cell death. Knockdown of ATF4 alleviated cartilage damage and reduced ferroptosis in both cell and mouse models. Mechanistically, ATF4 directly binds to the promoter of nuclear protein 1 (NUPR1) and activates its transcription. Overexpression of NUPR1 reversed the protective effects of ATF4 knockdown, confirming the critical role of the ATF4-NUPR1 axis in mediating ferroptosis and OA progression. These findings identify ATF4 as a key driver of OA via ferroptosis regulation and suggest that targeting the ATF4-NUPR1 pathway may offer a promising therapeutic strategy.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 3","pages":"100039"},"PeriodicalIF":3.2,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12356395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Podoplanin hetero-insufficiency mice with inflammation in the jejunum demonstrates a good animal model of congenital protein-losing enteropathy. Podoplanin异源不足小鼠空肠炎症是先天性失蛋白性肠病的良好动物模型。
IF 3.2 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-22 DOI: 10.1016/j.jphyss.2025.100031
Toshio Ohhashi, Nagaharu Tsukiji, Moyuru Hayashi, Tomomi Watanabe-Asaka, Mieko Takasaka, Daisuke Maejima, Katsue Suzuki-Inoue, Yoshiko Kawai
{"title":"Podoplanin hetero-insufficiency mice with inflammation in the jejunum demonstrates a good animal model of congenital protein-losing enteropathy.","authors":"Toshio Ohhashi, Nagaharu Tsukiji, Moyuru Hayashi, Tomomi Watanabe-Asaka, Mieko Takasaka, Daisuke Maejima, Katsue Suzuki-Inoue, Yoshiko Kawai","doi":"10.1016/j.jphyss.2025.100031","DOIUrl":"10.1016/j.jphyss.2025.100031","url":null,"abstract":"<p><p>We have identified the Podoplanin expression in rat jejunal villi. We aimed to investigate the relationship between the Podoplanin expression in jejunal villi and the pathogenesis of congenital protein-losing enteropathy (PLE), using the Podoplanin heterozygous knock-out (Pdpn-het KO) mice and aspirin-induced inflammation of the jejunum. In the Pdpn-het KO mice the reticular and complexes distribution of Podoplanin was observed in the jejunal villi, resulting in be swollen of lamina propria. To confirm the abnormal distribution of small lymph vessels in the jejunal villi, the LYVE-1 immunohistochemical expression was investigated. The expression of Podoplanin and LYVE-1 in the jejunum of the Pdpn-het KO mice exhibited a distinct pattern. The intravenous administration of Evans blue dye appeared quickly into the mesenteric lymph vessels and lymph nodes in the wild-type but not observed in Pdpn-het KO mice. In the Pdpn-het KO mice, aspirin-induced jejunal inflammation produced a significant leakage of the intravenous administration of FITC-albumin into the jejunal lumen. The hypoalbuminemia in the blood and the marked distribution of FITC-albumin in the jejunal villi were also observed in the mice. In conclusion, we proposed that Pdpn-het KO mice with jejunal inflammation demonstrates a good animal model of the congenital PLE.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 3","pages":"100031"},"PeriodicalIF":3.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Heart rate changes related to risky selections and outcomes in rat gambling tasks. 大鼠赌博任务中与风险选择和结果相关的心率变化。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-01 Epub Date: 2025-04-10 DOI: 10.1016/j.jphyss.2025.100022
Fumiya Fukushima, Atsushi Tamura, Nahoko Kuga, Takuya Sasaki
{"title":"Heart rate changes related to risky selections and outcomes in rat gambling tasks.","authors":"Fumiya Fukushima, Atsushi Tamura, Nahoko Kuga, Takuya Sasaki","doi":"10.1016/j.jphyss.2025.100022","DOIUrl":"10.1016/j.jphyss.2025.100022","url":null,"abstract":"<p><p>Risk-taking behavior is crucial to increase potential outcomes and alter arousal states in the brain and body represented by heart rates. In this study, we monitored changes in heart rate as rats performed a 50:50 gambling task in which they selected either a certain outcome with 100 % probability (sure option) or a double outcome with 50 % probability (risky option). When rats selected risky options, they exhibited significantly greater decreases in their heart rates before selection than when they selected certain options. In addition, we observed significantly larger increases in heart rates when the rats recognized larger outcomes after selecting the risky options than the sure options. Similar dynamic changes in heart rates were observed in a 25:75 gambling condition with different reward magnitudes and probabilities. These results demonstrate that animals can dynamically alter their heart rates in response to risky selection and outcomes.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 2","pages":"100022"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12018179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Editorial: Special issue on thermosensitive TRP channels. 社论:关于热敏TRP通道的特刊。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-01 Epub Date: 2025-03-29 DOI: 10.1016/j.jphyss.2025.100020
Makoto Tominaga
{"title":"Editorial: Special issue on thermosensitive TRP channels.","authors":"Makoto Tominaga","doi":"10.1016/j.jphyss.2025.100020","DOIUrl":"10.1016/j.jphyss.2025.100020","url":null,"abstract":"","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 2","pages":"100020"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12018543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Extending wave propagation along muscle fibers originates from early local contraction at the end-plate region. 延伸波沿肌纤维的传播源于端板区域的早期局部收缩。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-01 Epub Date: 2025-05-09 DOI: 10.1016/j.jphyss.2025.100023
Tomonori Hayashi, Naoya Nakahara, Shigeru Morimoto, Maki Yamaguchi, Kazuhiro Hirano, Shigeru Takemori
{"title":"Extending wave propagation along muscle fibers originates from early local contraction at the end-plate region.","authors":"Tomonori Hayashi, Naoya Nakahara, Shigeru Morimoto, Maki Yamaguchi, Kazuhiro Hirano, Shigeru Takemori","doi":"10.1016/j.jphyss.2025.100023","DOIUrl":"10.1016/j.jphyss.2025.100023","url":null,"abstract":"<p><p>We investigated the propagation of extending waves along twitching muscle fibers triggered by the internal shortening of early local contraction in the end-plate region. Bullfrog sartorius muscles were minimally stimulated, and the displacement of carbon particles attached to the muscle surface was captured using a high-speed camera. We found an extending wave along the fiber at a velocity of 5.35 ± 0.33 m·s⁻¹, faster than the conduction of action potentials at 3.04 ± 0.31 m·s⁻¹. Local compression of the muscle surface blocked the propagation of the extending wave, indicating its mechanical nature. Muscle stretching increased the extending wave velocity. These findings provide direct evidence that mechanically transmitted extending waves originate from early local contractions in the end-plate region and propagate along muscle fibers ahead of the contraction wave.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 2","pages":"100023"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Influence of endurance versus resistance exercise training on central and peripheral chemoreflexes in young healthy individuals. 耐力和阻力运动训练对年轻健康个体中枢和外周化学反射的影响。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-01 Epub Date: 2025-05-15 DOI: 10.1016/j.jphyss.2025.100027
Thalia Babbage, Ana L C Sayegh, Jui-Lin Fan, Nicholas Gant, Julian F R Paton, James P Fisher
{"title":"Influence of endurance versus resistance exercise training on central and peripheral chemoreflexes in young healthy individuals.","authors":"Thalia Babbage, Ana L C Sayegh, Jui-Lin Fan, Nicholas Gant, Julian F R Paton, James P Fisher","doi":"10.1016/j.jphyss.2025.100027","DOIUrl":"10.1016/j.jphyss.2025.100027","url":null,"abstract":"<p><p>Heightened central and peripheral chemoreflex sensitivity are associated with poor outcomes, but therapeutic approaches to target them are lacking. Endurance and resistance exercise training improve a multitude of physiological outcomes, but their effects on ventilatory chemoreflex sensitivity are unclear. Accordingly, the cardiorespiratory responses to steady-state isocapnic hypoxia (10 % O<sub>2</sub>, 5-minutes) and hyperoxic hypercapnic rebreathing (5 % CO<sub>2</sub>-95 % O<sub>2</sub>) were compared in endurance, resistance, and untrained groups. Central chemoreflex sensitivity was taken as the slope of the relationship between minute ventilation (V̇<sub>E</sub>) and end-tidal partial pressure of CO<sub>2</sub>. Peripheral chemoreflex sensitivity was determined from the absolute increase in V̇<sub>E</sub> from baseline to peak V̇<sub>E</sub> expressed relative to the fall in oxygen saturation. Neither central (P = 0.093) nor peripheral (P = 0.847) ventilatory chemoreflex sensitivities were different between groups. Future investigations should seek to understand whether exercise training modality influences central and peripheral chemoreflex sensitivity in older and clinical populations.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 2","pages":"100027"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Xanthine oxidase inhibitor allopurinol preserves cardiac function after experimental malocclusion induced by occlusal disharmony in mice. 黄嘌呤氧化酶抑制剂别嘌呤醇对小鼠咬合不协调所致实验性错颌合的心脏功能有保护作用。
IF 2.6 4区 医学
Journal of Physiological Sciences Pub Date : 2025-07-01 Epub Date: 2025-06-29 DOI: 10.1016/j.jphyss.2025.100029
Takao Mitsubayashi, Kenji Suita, Yoshiki Ohnuki, Misao Ishikawa, Aiko Ito, Ichiro Matsuo, Go Miyamoto, Mariko Abe, Akinaka Morii, Yasumasa Mototani, Megumi Nariyama, Ren Matsubara, Yoshio Hayakawa, Satoshi Okumura
{"title":"Xanthine oxidase inhibitor allopurinol preserves cardiac function after experimental malocclusion induced by occlusal disharmony in mice.","authors":"Takao Mitsubayashi, Kenji Suita, Yoshiki Ohnuki, Misao Ishikawa, Aiko Ito, Ichiro Matsuo, Go Miyamoto, Mariko Abe, Akinaka Morii, Yasumasa Mototani, Megumi Nariyama, Ren Matsubara, Yoshio Hayakawa, Satoshi Okumura","doi":"10.1016/j.jphyss.2025.100029","DOIUrl":"10.1016/j.jphyss.2025.100029","url":null,"abstract":"<p><p>Oxidative stress caused by poor oral condition is associated with systemic diseases, including cardiovascular disease. In this work, therefore, we examined the effect of allopurinol, an inhibitor of the reactive oxygen species (ROS)-producing enzyme xanthine oxidase, on cardiac dysfunction in our bite-opening (BO) mouse model, in which a suitable appliance is cemented onto the mandibular incisior. After two weeks, we confirmed that cardiac function was significantly decreased in the BO group compared to the control, while allopurinol ameliorated the dysfunction. The impairment of cardiac function in BO mice was associated with increased production of ROS by xanthine oxidase, leading to the activation of calmodulin kinase II, and altered phosphorylation of ryanodine receptor 2 and phospholamban. These changes were also suppressed by allopurinol. Our results suggest that oxidative stress might play an important role in the development of cardiac dysfunction, and further indicate that allopurinol is protective against BO-induced cardiac dysfunction.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"75 2","pages":"100029"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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