Journal of Clinical Biochemistry and Nutrition最新文献_第9页

Erratum. 勘误表。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 DOI: 10.3164/jcbn.24-178_Erratum2

引用次数: 0

Simple method for estimating low muscle mass in persons with bioelectrical impedance analysis measurement difficulties. 有生物电阻抗分析测量困难的人低肌肉量的简单估计方法。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-20 DOI: 10.3164/jcbn.25-13

Hirohito Sasaki, Osamu Yamamura, Hidenori Onishi, Hiromasa Tsubouchi, Yasutaka Mizukami, Masafumi Kubota, Ryouko Ikeda, Naohiro Konoshita, Tokuharu Tanaka, Takahiro Kishimoto, Koji Kobayashi, Hiroyuki Hayashi, Yasuhiro Nishiyama

{"title":"Simple method for estimating low muscle mass in persons with bioelectrical impedance analysis measurement difficulties.","authors":"Hirohito Sasaki, Osamu Yamamura, Hidenori Onishi, Hiromasa Tsubouchi, Yasutaka Mizukami, Masafumi Kubota, Ryouko Ikeda, Naohiro Konoshita, Tokuharu Tanaka, Takahiro Kishimoto, Koji Kobayashi, Hiroyuki Hayashi, Yasuhiro Nishiyama","doi":"10.3164/jcbn.25-13","DOIUrl":"10.3164/jcbn.25-13","url":null,"abstract":"Bioelectrical impedance analysis cannot be used to measure muscle mass in some individuals. We aimed to determine cutoff values for low skeletal muscle mass index in sarcopenia diagnosis, based on the fat-free muscle mass index estimated using body fat percentage prediction equations, without relying on bioelectrical impedance analysis. The study included 564 residents from Wakasa, Fukui Prefecture, with a mean age of 76.0 ± 7.1 years. Body composition assessments using bioelectrical impedance analysis were conducted. Three prediction equations for body fat percentage (Ito et al., Deurenberg et al., and Gallagher et al.'s model for Asians) were applied. The cutoff value of the fat-free muscle mass index corresponding to low skeletal muscle mass index in sarcopenia diagnostic criteria was determined using receiver operating characteristic curves. Receiver operating characteristic curve analysis showed that the formula by Ito et al. yielded the highest area under the curve for estimating low skeletal muscle mass index in men, at 0.83. In women, the formulas by Ito et al. and Gallagher et al. performed similarly, each achieving an area under the curve of 0.779. The fat-free muscle mass index estimated using the body fat prediction formulas appear to be useful for screening low skeletal muscle mass index.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"91-98"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799259","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

The revelation of UCHL1 in malignant epithelial cells of TNBC reinforcing cisplatin resistance by modulating ferroptosis based on single-cell transcriptome data. 基于单细胞转录组数据的TNBC恶性上皮细胞中UCHL1通过调节铁凋亡增强顺铂耐药的揭示。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-15 DOI: 10.3164/jcbn.24-206

Huan Li, Shaojun Chen, Haiqin Hou, Zhuoying Li, Yiming Zhang, Wenxia Zhang

{"title":"The revelation of UCHL1 in malignant epithelial cells of TNBC reinforcing cisplatin resistance by modulating ferroptosis based on single-cell transcriptome data.","authors":"Huan Li, Shaojun Chen, Haiqin Hou, Zhuoying Li, Yiming Zhang, Wenxia Zhang","doi":"10.3164/jcbn.24-206","DOIUrl":"10.3164/jcbn.24-206","url":null,"abstract":"Chemotherapy resistance is a key obstacle in the treatment of triple-negative breast cancer (TNBC). Single-cell RNA sequencing (scRNA-seq) plays a pivotal part in revealing the mechanism of drug resistance in tumors. This work aimed to explore the molecular events driving TNBC resistance based on scRNA-seq data. Breast cancer (BC) scRNA-seq data GSE176078 was sourced from the GEO database. Nine TNBC samples were analyzed. The cellular composition and differentially expressed genes of TNBC were clarified through dimension reduction, clustering, and cell annotation. Drug-resistant and sensitive epithelial cell clusters in malignant epithelial cells were identified, with their heterogeneity analyzed. Key genes driving drug-resistant epithelium were screened and KEGG enrichment analysis was undertaken. The expression of Ubiquitin Carboxy-Terminal Hydrolase L1 (UCHL1) in TNBC was examined. The effect and molecular mechanism of UCHL1 on cisplatin (CDDP) resistance in TNBC was confirmed by constructing CDDP-resistant cell lines. We successfully identified resistant and sensitive cell clusters in malignant epithelial cells of TNBC and screened for the greatly upregulated gene UCHL1 in the resistant epithelium. KEGG analysis revealed its enrichment in the ferroptosis signaling pathway. Further analyses demonstrated the upregulation of UCHL1 in CDDP-resistant TNBC cells. Knocking down UCHL1 potentiated the sensitivity of TNBC cells to CDDP treatment and reinforced ferroptosis. The ferroptosis inhibitor Ferrostatin-1 reversed the inhibitory effect of UCHL1 knockdown on CDDP resistance. UCHL1 reinforces CDDP resistance in TNBC by suppressing ferroptosis. The study brings new insights into the drug-resistance mechanism of TNBC.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"18-29"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799261","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

Sanguinarine attenuates hypoxia/reoxygenation-triggered H9c2 cell injury through activation of the Nrf2/NLRP3 pathway. 血根碱通过激活Nrf2/NLRP3通路减轻缺氧/再氧化引发的H9c2细胞损伤。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-11 DOI: 10.3164/jcbn.24-235

Bo Qiu, Xin Li, Wenna Wang

{"title":"Sanguinarine attenuates hypoxia/reoxygenation-triggered H9c2 cell injury through activation of the Nrf2/NLRP3 pathway.","authors":"Bo Qiu, Xin Li, Wenna Wang","doi":"10.3164/jcbn.24-235","DOIUrl":"10.3164/jcbn.24-235","url":null,"abstract":"Myocardial ischemia/reperfusion injury (MI/RI) is a prevalent condition encountered by many patients with ischemic heart disease, which can badly influence the health of patients and even do harm their lives. Sanguinarine (SA), one active ingredient separated from the poppy family, and exhibits anti-oxidant, anti-tumor, and anti-inflammation properties. However, the precise regulatory impacts and associated mechanisms of SA in the progression of MI/RI remain largely elusive. In this study, firstly, H9c2 cells were treated by hypoxia/reoxygenation (HR) to mimic MI/RI cell model. It was uncovered that SA strengthened HR-mediated cell viability of H9c2 cells. Following HR treatment, there was an increase in the production of inflammatory markers (TNF-α, IL-1β, and IL-6), whereas this effect was mitigated after SA treatment. The oxidative stress was heightened after HR treatment, but this phenomenon was offset after SA treatment. SA activated the Nrf2/NLRP3 pathway and relieved proptosis. At last, through rescue assays, it was demonstrated that SA improved HR-triggered inflammation and oxidative stress through Nrf2 pathway. SA also modulated HR-triggered cell viability, inflammation, and oxidative stress in rat primary cardiomyocytes. In summary, our findings indicate that SA protects against HR-induced H9c2 cell injury through activation of the Nrf2/NLRP3 pathway. This discovery suggests that SA may be one helpful drug for ameliorating MI/RI.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"37-44"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799257","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

Seven days of piceatannol supplementation exerted no effect on fat metabolism at rest, during and after exercise. 在休息、运动期间和运动后，补充7天皮杉醇对脂肪代谢没有影响。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-11 DOI: 10.3164/jcbn.25-2

Nobukazu Kasai, Kanon Hayashi, Masaki Kito, Takuma Morishima

{"title":"Seven days of piceatannol supplementation exerted no effect on fat metabolism at rest, during and after exercise.","authors":"Nobukazu Kasai, Kanon Hayashi, Masaki Kito, Takuma Morishima","doi":"10.3164/jcbn.25-2","DOIUrl":"10.3164/jcbn.25-2","url":null,"abstract":"Piceatannol is a type of polyphenol that is abundantly obtained from passion fruit. The present study aimed to determine the effect of 7 days of piceatannol supplementation on fat metabolism at rest, during and after low-intensity aerobic exercise. This randomized, double-blind, and crossover study included eight physically active male participants. The participants completed two experimental trials: placebo and piceatannol. They ingested either a placebo or piceatannol tablets containing 0 or 10 ‍mg of piceatannol for seven consecutive days. The participants visited the laboratory at 8:00 am after seven days. In the following baseline measurements, the participants performed 60 ‍min of pedaling exercise at 30% of their maximum oxygen uptake. Respiratory gas and blood samples were collected before, during, and after the exercise. No significant differences were found between the trials in oxygen uptake, carbon dioxide output, ventilation, and respiratory exchange ratio either at rest and during and after exercise. Similarly, serum growth hormone, cortisol, insulin, free fatty acid, glycerol, acetoacetic acid, 3-hydroxybutyric acid, and ketone body responses exhibited no significant differences between trials. These results indicate that the 7-day piceatannol supplementation did not promote fat metabolism at rest and during and after low-intensity aerobic exercise.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"85-90"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799258","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

Andrographolide derivative CX-10 alleviates ulcerative colitis by modulating autophagy and cellular stress. 穿心莲内酯衍生物CX-10通过调节自噬和细胞应激减轻溃疡性结肠炎。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-15 DOI: 10.3164/jcbn.24-203

Zhengshi Chen, Yongheng He, Yi Hong, Feng Yu, Tianyun Gong, Xiaoxiao Tong

{"title":"Andrographolide derivative CX-10 alleviates ulcerative colitis by modulating autophagy and cellular stress.","authors":"Zhengshi Chen, Yongheng He, Yi Hong, Feng Yu, Tianyun Gong, Xiaoxiao Tong","doi":"10.3164/jcbn.24-203","DOIUrl":"10.3164/jcbn.24-203","url":null,"abstract":"Ulcerative colitis (UC) is a debilitating inflammatory bowel disease that poses significant challenges in clinical management. Despite existing therapies, many patients fail to achieve adequate symptom relief, underscoring the need to address the underlying mechanisms contributing to the pathogenesis of UC. Andrographis paniculata has been extensively studied in traditional Chinese medicine for its anti-inflammatory properties. This study aimed to evaluate the effects of CX-10, a derivative of andrographolide, on autophagy, oxidative stress, and inflammation in UC. Using dextran sulfate sodium (DSS)-induced mouse model of UC, our findings demonstrated that CX-10 treatment resulted in significant reductions in body weight loss, Disease Activity Index (DAI), and histopathological injury scores, characterized by decreased inflammatory cell infiltration and mucosal damage compared to DSS-treated controls. Quantitative real-time PCR (qRT-PCR) revealed a marked restoration of autophagy-related genes Becn1 and Atg5 in CX-10-treated colonic tissues. Western blot analysis further confirmed enhanced autophagic flux, evidenced by significant increases in the LC3-II/I ratio. CX-10 treatment also led to reduced endoplasmic reticulum (ER) stress, indicated by decreases in the transcript and protein levels of GRP78 and CHOP. Consistent with the in vivo findings, in vitro studies demonstrated that CX-10 effectively enhanced autophagy and reduced oxidative stress in lipopolysaccharides (LPS)-treated HT-29 colonic epithelial cells and RAW 264.7 macrophages. This was accompanied by a marked decrease in reactive oxygen species (ROS) levels, as determined by DCFDA assays. In conclusion, CX-10 exerts protective effects against DSS-induced UC through modulation of autophagy and oxidative stress pathways, suggesting its potential as a novel therapeutic agent for managing UC.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"45-54"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799251","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

8-Prenylnaringenin suppresses obesity in high-fat diet-fed C57BL/6J mice via adiponectin secretion. 8- prenylnaringin通过脂联素分泌抑制高脂饮食C57BL/6J小鼠的肥胖。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-02-22 DOI: 10.3164/jcbn.24-214

Fukiko Okada, Akiko Kohara, Yuichi Ukawa, Rie Mukai, Hitoshi Ashida, Yoko Yamashita

{"title":"8-Prenylnaringenin suppresses obesity in high-fat diet-fed C57BL/6J mice via adiponectin secretion.","authors":"Fukiko Okada, Akiko Kohara, Yuichi Ukawa, Rie Mukai, Hitoshi Ashida, Yoko Yamashita","doi":"10.3164/jcbn.24-214","DOIUrl":"10.3164/jcbn.24-214","url":null,"abstract":"8-Prenylnaringenin (8-PN) is a prenylflavonoid found in hops (Humulus lupulus L.). It has several beneficial functions, which include the inhibition of bone loss and muscle atrophy. 8-PN is a metabolite of xanthohumol, which can prevent obesity in mice; however, the effect of 8-PN on obesity is still unknown. In the present study, we found that 8-PN prevented obesity in high-fat diet-fed mice. When C57BL6/J male mice were fed 8-PN at 0.0005% or 0.005% with a high-fat diet for 8 weeks, body weight gain, fat accumulation in adipose tissue, and fatty liver induced by the high-fat diet were prevented. In mice fed a high-fat diet and 8-PN, adenosine monophosphate-activated protein kinase (AMPK) was activated in visceral adipose tissue, which was accompanied by decreased expression of a fatty acid synthesis-related factor and increased expression of a mitochondrial biosynthesis-related factor downstream of AMPK. AMPK appeared to be activated by adiponectin secretion, which was associated with increased expression of adipocyte differentiation markers in mice fed a high-fat diet and 8-PN. For the first time, this study shows that 8-PN can prevent obesity in mice and that it is effective at low concentrations that humans could consume in their daily diet.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"64-73"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799250","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

FOXM1 transcriptionally activates NEIL3 to inhibit ferroptosis in lung adenocarcinoma cells. FOXM1转录激活NEIL3抑制肺腺癌细胞铁下垂。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-08 DOI: 10.3164/jcbn.24-136

Hailang Hou, Xinpu Geng, Xingxing Shao, Jindao Wang, Wan Xia, Huijie Chen

{"title":"FOXM1 transcriptionally activates NEIL3 to inhibit ferroptosis in lung adenocarcinoma cells.","authors":"Hailang Hou, Xinpu Geng, Xingxing Shao, Jindao Wang, Wan Xia, Huijie Chen","doi":"10.3164/jcbn.24-136","DOIUrl":"10.3164/jcbn.24-136","url":null,"abstract":"Lung adenocarcinoma (LUAD) is responsible for a substantial portion of cancer-related deaths, carrying a bleak treatment outlook. The application of ferroptosis-focused treatments has shown great potential. This research is committed to uncovering the molecular mechanisms by which Nei Like DNA Glycosylase 3 (NEIL3) impacts ferroptosis in LUAD, in the quest for robust biomarkers. Using The Cancer Genome Atlas database, qRT-PCR, and Western blot (WB), we evaluated the expression of NEIL3 in LUAD tissues and cells, then performed gene set enrichment analysis to identify enriched gene sets. Predictive tools hTFtarget and MoLoTool assisted in identifying potential upstream transcription factors and their promoter binding sites for NEIL3, following which we conducted Pearson correlation analysis. The binding affinity of NEIL3 to Forkhead box protein M1 (FOXM1) was validated with dual-luciferase and chromatin immunoprecipitation assays. Cell viability was determined by measuring MDA and Fe2+ content in cells with the aid of cell counting kit-8. Lipid reactive oxygen species (ROS) levels were detected by flow cytometry, and WB was employed to evaluate the expression of GPX4 and SLC7A11 proteins. An upregulation of NEIL3 is observed in LUAD tissues and cell lines, particularly within pathways linked to ferroptosis. When NEIL3 was knocked down, there was a decline in the viability of LUAD cells, coupled with elevated MDA, Fe2+, and lipid ROS levels. Protein expression of GPX4 and SLC7A11 was inhibited, but these phenotypes were rescued by the application of a ferroptosis inhibitor. FOXM1 could interact with the NEIL3 gene promoter, initiating its transcription. In the context of LUAD, the activation of NEIL3 by FOXM1 constitutes the FOXM1/NEIL3 axis that counteracts ferroptosis in LUAD cells.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"10-17"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799253","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

Enteral nutrition intervention improves intestinal ischemia-reperfusion injury by modulating the SENP1/SIRT3 axis. 肠内营养干预通过调节SENP1/SIRT3轴改善肠缺血再灌注损伤。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-09 DOI: 10.3164/jcbn.25-31

Shizhuang Wei, Zhenhua Li, Bo Wen, Wei Wang, Daolai Huang, Chao Zhang, Xianghua Wu

{"title":"Enteral nutrition intervention improves intestinal ischemia-reperfusion injury by modulating the SENP1/SIRT3 axis.","authors":"Shizhuang Wei, Zhenhua Li, Bo Wen, Wei Wang, Daolai Huang, Chao Zhang, Xianghua Wu","doi":"10.3164/jcbn.25-31","DOIUrl":"10.3164/jcbn.25-31","url":null,"abstract":"Intestinal ischemia-reperfusion (II/R) injury is a significant clinical concern with high mortality rates. Mitochondria play a crucial role in this process, and maintaining mitochondrial homeostasis is a potential treatment target. SENP1 is a de-SUMOylated hydrolase that may regulate SIRT3, a major mitochondrial deacetylase. However, the role of SENP1 and SIRT3 in II/R remains unclear. Employing a combination of in vitro cell culture experiments utilizing Caco-2 cells and in vivo II/R models with SD rats, along with an array of molecular biology techniques such as gene silencing, protein detection methods, immunoprecipitation, histological analysis, and functional assays, this study delved into the role of SENP1 and SIRT3 in intestinal ischemia-reperfusion injury. Statistical analysis was meticulously conducted to evaluate the significance of the obtained results. SENP1 and SIRT3 are co-expressed and interact in Caco-2 cells. In models of II/R, the expression of SENP1 increased while that of SIRT3 decreased. Reducing SENP1 expression by siRNA or enteral nutrition intervention with bupropion alleviated intestinal II/R injury, reduced mitochondrial damage and oxidative stress, and improved the number and function of mitochondria. Our study demonstrates the importance of SENP1 and SIRT3 in intestinal ischemia-reperfusion injury. Reducing SENP1 expression through siRNA or enteral nutrition intervention shows promise as a potential therapeutic approach. This research provides new insights into the mechanism of II/R injury and paves the way for further investigations.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"55-63"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799252","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

Levosimendan alleviates myocardial ischemia-reperfusion injury by regulating mitochondrial autophagy through cGAS-STING signaling pathway. 左西孟旦通过cGAS-STING信号通路调节线粒体自噬，减轻心肌缺血再灌注损伤。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-18 DOI: 10.3164/jcbn.25-8

Feng Shi, Han Bao, Fanqing Meng, Yunting Pang

{"title":"Levosimendan alleviates myocardial ischemia-reperfusion injury by regulating mitochondrial autophagy through cGAS-STING signaling pathway.","authors":"Feng Shi, Han Bao, Fanqing Meng, Yunting Pang","doi":"10.3164/jcbn.25-8","DOIUrl":"10.3164/jcbn.25-8","url":null,"abstract":"Levosimendan, a calcium sensitizer, has cardioprotective effects against myocardial ischemia-reperfusion injury (MIRI). Mitophagy plays an important role in MIRI, and the cGAS-STING signaling pathway can participate in mitophagy in a variety of ways. The purpose of this study was to explore the new molecular mechanism by which levosimendan exerts cardioprotective effects in order to provide a new experimental basis for the clinical application of levosimendan. In this study, an isolated MIRI rat model was established, and 48 rats were randomly divided into four groups (n = 12): continuous perfusion group (Group C), ischemia-reperfusion group (IR group), ischemia-reperfusion + levosimendan group (IR + L group), and ischemia-reperfusion + levosimendan + sting activator group (IR + LA group). The hemodynamic indices, myocardial infarction volume, expression of cGAS-STING signaling pathway proteins, and mitophagy-related proteins in isolated rat hearts of the four groups were compared. This study showed that levosimendan can reduce the level of myocardial mitophagy in ischemia-reperfusion rats by inhibiting the cGAS-STING signaling pathway, reducing myocardial injury, and playing a myocardial protective role.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"74-78"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799255","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