Journal of physiology and biochemistry最新文献_第10页

Quercetin improved hepatic circadian rhythm dysfunction in middle-aged mice fed with vitamin D-deficient diet. 槲皮素改善了喂食维生素D缺乏饮食的中年小鼠的肝脏昼夜节律功能障碍。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-02-01 Epub Date: 2023-11-10 DOI: 10.1007/s13105-023-00990-0

Rui Li, Guiping Wang, Ruitong Liu, Lan Luo, Ying Zhang, Zhongxiao Wan

{"title":"Quercetin improved hepatic circadian rhythm dysfunction in middle-aged mice fed with vitamin D-deficient diet.","authors":"Rui Li, Guiping Wang, Ruitong Liu, Lan Luo, Ying Zhang, Zhongxiao Wan","doi":"10.1007/s13105-023-00990-0","DOIUrl":"10.1007/s13105-023-00990-0","url":null,"abstract":"We aimed to determine whether quercetin is capable of improving circadian rhythm and metabolism disorder under vitamin D-deficient condition. Middle-aged mice were randomly divided into four groups, namely, control (CON), vitamin D-deficient diet (VDD), quercetin (Q), and quercetin intervention in vitamin D-deficient diet (VDQ), with a total of 12 weeks' intervention. Mice were sacrificed at zeitgeber time1 (ZT1) and ZT13 time points. At ZT1, circadian locomotor output cycle kaput (CLOCK) protein expression from VDD, Q, and VDQ groups; CRY1 from Q group; and CRY2 from VDD group were significantly lower compared to CON group. The mRNA expression of Sirt1, Bmal1, Clock, Cry1, and Cry2 in VDQ groups, also Bmal1, Clock, and Cry1 from Q group, were significantly decreased compared to CON group. At ZT13, compared to CON group, fasting insulin and homeostasis model assessment-insulin resistance (HOMA-IR) were higher in VDD group; BMAL1 was significantly increased, while CLOCK and CRY1 protein were significantly decreased from VDD group; CLOCK protein from VDQ group was significantly higher compared to CON, VDD, and Q groups, and also, BMAL1 protein expression from VDQ group was elevated compared to CON group. The mRNA expression of Bmal1, Clock, Per2, Cry1, and Cry2 in VDQ groups were significantly increased compared to CON groups. The mRNA expression of Bmal1 from VDQ group was decreased compared to both VDD and Q group. In conclusion, vitamin D-deficient diet resulted in a disordered liver circadian rhythm, and quercetin improved the hepatic circadian desynchronization. Quercetin supplementation might be effective for balancing circadian rhythm under vitamin D-deficient condition.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"137-147"},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72014609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Deciphering the roles of triiodothyronine (T3) and thyroid-stimulating hormone (TSH) on cardiac electrical remodeling in clinical and experimental hypothyroidism. 解读三碘甲状腺原氨酸(T3)和促甲状腺激素(TSH)在临床和实验甲状腺功能减退患者心电重构中的作用。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-02-01 Epub Date: 2023-11-29 DOI: 10.1007/s13105-023-01000-z

Oscar Casis, Leire Echeazarra, Beatriz Sáenz-Díez, Mónica Gallego

{"title":"Deciphering the roles of triiodothyronine (T3) and thyroid-stimulating hormone (TSH) on cardiac electrical remodeling in clinical and experimental hypothyroidism.","authors":"Oscar Casis, Leire Echeazarra, Beatriz Sáenz-Díez, Mónica Gallego","doi":"10.1007/s13105-023-01000-z","DOIUrl":"10.1007/s13105-023-01000-z","url":null,"abstract":"Hypothyroidism is the most frequent endocrine pathology. Although clinical or overt hypothyroidism has been traditionally associated to low T3 / T4 and high thyrotropin (TSH) circulating levels, other forms exist such as subclinical hypothyroidism, characterized by normal blood T3 / T4 and high TSH. In its different forms is estimated to affect approximately 10% of the population, especially women, in a 5:1 ratio with respect to men. Among its consequences are alterations in cardiac electrical activity, especially in the repolarization phase, which is accompanied by an increased susceptibility to cardiac arrhythmias. Although these alterations have traditionally been attributed to thyroid hormone deficiency, recent studies, both clinical trials and experimental models, demonstrate a fundamental role of TSH in cardiac electrical remodeling. Thus, both metabolic thyroid hormones and TSH regulate cardiac ion channel expression in many and varied ways. This means that the different combinations of hormones that predominate in different types of hypothyroidism (overt, subclinic, primary, central) can generate different forms of cardiac electrical remodeling. These new findings are raising the relevant question of whether serum TSH reference ranges should be redefined.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"1-9"},"PeriodicalIF":3.7,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10808292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

N6-methyladenosine in myeloid cells: a novel regulatory factor for inflammation-related diseases 髓系细胞中的 N6-甲基腺苷：炎症相关疾病的新型调节因子

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-12-30 DOI: 10.1007/s13105-023-01002-x

Jin Pang, Tong-dong Kuang, Xin-yuan Yu, Petr Novák, Yuan Long, Min Liu, Wei-qian Deng, Xiao Zhu, Kai Yin

{"title":"N6-methyladenosine in myeloid cells: a novel regulatory factor for inflammation-related diseases","authors":"Jin Pang, Tong-dong Kuang, Xin-yuan Yu, Petr Novák, Yuan Long, Min Liu, Wei-qian Deng, Xiao Zhu, Kai Yin","doi":"10.1007/s13105-023-01002-x","DOIUrl":"https://doi.org/10.1007/s13105-023-01002-x","url":null,"abstract":"N6-methyladenosine (m6A) is one of the most abundant epitranscriptomic modifications on eukaryotic mRNA. Evidence has highlighted that m6A is altered in response to inflammation-related factors and it is closely associated with various inflammation-related diseases. Multiple subpopulations of myeloid cells, such as macrophages, dendritic cells, and granulocytes, are crucial for the regulating of immune process in inflammation-related diseases. Recent studies have revealed that m6A plays an important regulatory role in the functional of multiple myeloid cells. In this review, we comprehensively summarize the function of m6A modification in myeloid cells from the perspective of myeloid cell production, activation, polarization, and migration. Furthermore, we discuss how m6A-mediated myeloid cell function affects the progression of inflammation-related diseases, including autoimmune diseases, chronic metabolic diseases, and malignant tumors. Finally, we discuss the challenges encountered in the study of m6A in myeloid cells, intended to provide a new direction for the study of the pathogenesis of inflammation-related diseases.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"10 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139068827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of exercise, metformin, and combination treatments on type 2 diabetic mellitus-induced muscle atrophy in db/db mice: Crosstalk between autophagy and the proteasome 运动、二甲双胍和联合疗法对 2 型糖尿病诱导的 db/db 小鼠肌肉萎缩的影响：自噬与蛋白酶体之间的相互影响

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-12-19 DOI: 10.1007/s13105-023-01001-y

Mengqi Xiang, Xinmeng Yuan, Nianyun Zhang, Liumei Zhang, Yuting Liu, Jingjing Liu, Yaran Gao, Ye Xu, Wen Sun, Qiang Tang, Yuan Zhang, Jiao Lu

{"title":"Effects of exercise, metformin, and combination treatments on type 2 diabetic mellitus-induced muscle atrophy in db/db mice: Crosstalk between autophagy and the proteasome","authors":"Mengqi Xiang, Xinmeng Yuan, Nianyun Zhang, Liumei Zhang, Yuting Liu, Jingjing Liu, Yaran Gao, Ye Xu, Wen Sun, Qiang Tang, Yuan Zhang, Jiao Lu","doi":"10.1007/s13105-023-01001-y","DOIUrl":"https://doi.org/10.1007/s13105-023-01001-y","url":null,"abstract":"Both exercise and metformin are common effective clinical treatments of type 2 diabetic mellitus. This study investigated the functional role of exercise, metformin, and combination treatment on type 2 diabetic mellitus–induced muscle atrophy. In this experiment, a total of 10 BKS mice were set as the control group. A total of 40 BKS-db/db mice were randomly divided into the control group (db/db); the exercise intervention group (db/db + Ex), which ran on a treadmill at 7–12 m/min, 30–40 min/day, 5 days/week; the metformin administration group (db/db + Met), which was administered 300 mg/kg of metformin solution by gavage daily; and the exercise combined with metformin administration group (db/db + Ex + Met). After 8 weeks of intervention, their tibialis anterior muscles were removed. The levels of insulin signaling pathway proteins, ubiquitin proteasome, and autophagic lysosome–associated proteins were detected using western blot, the expression of MuRF1 and Atrogin-1 was detected using immunohistochemical staining, and the degradation of autophagosomes was detected using double-labeled immunofluorescence. The db/db mice exhibited reduced insulin sensitivity and inhibition of the autophagic–lysosome system, the ubiquitin–proteasome system was activated, and protein degradation was exacerbated, leading to skeletal muscle atrophy. Exercise and metformin and their combined interventions can increase insulin sensitivity, whereas exercise alone showed more effective in inhibiting the ubiquitin–proteasome system, improving autophagy levels, and alleviating skeletal muscle atrophy. Compared with metformin, exercise demonstrated superior improvement of muscle atrophy by promoting the synthesis and degradation of autophagy through the AMPK/ULK1 pathway. However, the combination treatment exhibits no synergistic effect on muscle atrophy.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"17 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138743563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ERG mediates the inhibition of NK cell cytotoxicity through the HLX/STAT4/Perforin signaling pathway, thereby promoting the progression of myocardial infarction ERG 通过 HLX/STAT4/Perforin 信号通路介导对 NK 细胞细胞毒性的抑制，从而促进心肌梗死的进展

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-12-13 DOI: 10.1007/s13105-023-00999-5

Liang Guo, Di Wu, Jianfen Shen, Yuan Gao

{"title":"ERG mediates the inhibition of NK cell cytotoxicity through the HLX/STAT4/Perforin signaling pathway, thereby promoting the progression of myocardial infarction","authors":"Liang Guo, Di Wu, Jianfen Shen, Yuan Gao","doi":"10.1007/s13105-023-00999-5","DOIUrl":"https://doi.org/10.1007/s13105-023-00999-5","url":null,"abstract":"This study aimed to investigate the role of ERG in the HLX/STAT4/Perforin signaling axis, impacting natural killer (NK) cell cytotoxicity and myocardial infarction (MI) progression. NK cell cytotoxicity was assessed via co-culture and 51Cr release assays. Datasets GSE34198 and GSE97320 identified common differentially expressed genes in MI. NK cell gene expression was analyzed in MI patients and healthy individuals using qRT-PCR and Western blotting. ERG's regulation of HLX and STAT4's regulation of perforin were studied through computational tools (MEM) and ChIP experiments. HLX's influence on STAT4 was explored with the MG132 proteasome inhibitor. Findings were validated in a mouse MI model.ERG, a commonly upregulated gene, was identified in NK cells from MI patients and mice. ERG upregulated HLX, leading to STAT4 proteasomal degradation and reduced Perforin expression. Consequently, NK cell cytotoxicity decreased, promoting MI progression. ERG mediates the HLX/STAT4/Perforin axis to inhibit NK cell cytotoxicity, fostering MI progression. These results provide vital insights into MI's molecular mechanisms.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"146 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138631271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Binge drinking leads to an oxidative and metabolic imbalance in skeletal muscle during adolescence in rats: endocrine repercussion. 酗酒导致青春期大鼠骨骼肌氧化和代谢失衡:内分泌反应。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-11-01 Epub Date: 2023-09-07 DOI: 10.1007/s13105-023-00983-z

Inés Romero-Herrera, Fátima Nogales, Javier Diaz-Castro, Jorge Moreno-Fernandez, María Del Carmen Gallego-Lopez, Julio J Ochoa, Olimpia Carreras, María Luisa Ojeda

{"title":"Binge drinking leads to an oxidative and metabolic imbalance in skeletal muscle during adolescence in rats: endocrine repercussion.","authors":"Inés Romero-Herrera, Fátima Nogales, Javier Diaz-Castro, Jorge Moreno-Fernandez, María Del Carmen Gallego-Lopez, Julio J Ochoa, Olimpia Carreras, María Luisa Ojeda","doi":"10.1007/s13105-023-00983-z","DOIUrl":"10.1007/s13105-023-00983-z","url":null,"abstract":"Binge drinking (BD) is an especially pro-oxidant model of alcohol consumption, mainly used by adolescents. It has recently been related to the hepatic IR-process. Skeletal muscle is known to be involved in insulin action and modulation through myokine secretion. However, there is no information on muscle metabolism and myokine secretion after BD exposure in adolescents. Two experimental groups of adolescent rats have been used: control and BD-exposed one. Oxidative balance, energy status and lipid, and protein metabolism have been analyzed in muscle, together with myokine serum levels (IL-6, myostatin, LIF, IL-5, fractalkine, FGF21, irisin, BDNF, FSTL1, apelin, FABP3, osteocrin, osteonectin (SPARC), and oncostatin). In muscle, BD affects the antioxidant enzyme balance leading to lipid and protein oxidation. Besides, it also increases the activation of AMPK and thus contributes to decrease SREBP1 and pmTOR and to increase FOXO3a expressions, promoting lipid and protein degradation. These alterations deeply affect the myokine secretion pattern. This is the first study to examine a general myokine response after exposure to BD. BD not only caused a detrimental imbalance in myokines related to muscle turnover, decreased those contributing to increase IR-process, decreased FST-1 and apelin and their cardioprotective function but also reduced the neuroprotective BDNF. Consequently, BD leads to an important metabolic and energetic disequilibrium in skeletal muscle, which contributes to exacerbate a general IR-process.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"799-810"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10525029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Involvement of histone methylation in the regulation of neuronal death. 组蛋白甲基化参与神经元死亡的调控。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-11-01 Epub Date: 2023-08-07 DOI: 10.1007/s13105-023-00978-w

Lei Zhang, Tai Zhou, Yaxin Su, Li He, Zhongcheng Wang

{"title":"Involvement of histone methylation in the regulation of neuronal death.","authors":"Lei Zhang, Tai Zhou, Yaxin Su, Li He, Zhongcheng Wang","doi":"10.1007/s13105-023-00978-w","DOIUrl":"10.1007/s13105-023-00978-w","url":null,"abstract":"Neuronal death occurs in various physiological and pathological processes, and apoptosis, necrosis, and ferroptosis are three major forms of neuronal death. Neuronal apoptosis, necrosis, and ferroptosis are widely identified to involve the progress of stroke, Parkinson's disease, and Alzheimer's disease. A growing body of evidence has pointed out that neuronal death is tightly associated with expression of related genes and alteration of signaling molecules. In addition, recently, epigenetics has been increasingly focused on as a vital regulatory mechanism for neuronal apoptosis, necrosis, and ferroptosis, providing a new direction for treating nervous system diseases. Moreover, growing researches suggest that histone methylation or demethylation is involved in the processes of neuronal apoptosis, necrosis, and ferroptosis. These researches may imply that studying the potential roles of histone methylation is essential for treating the nervous system diseases. Here, we review potential roles of histone methylation and demethylation in neuronal death, which may give us a new direction in treating the nervous system diseases.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"685-693"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9937408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endothelial NOX5 overexpression induces changes in the cardiac gene profile: potential impact in myocardial infarction? 内皮细胞NOX5过表达诱导心脏基因谱改变:对心肌梗死的潜在影响?

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-11-01 Epub Date: 2023-08-11 DOI: 10.1007/s13105-023-00975-z

Adriana Cortés, Javier Marqués, Álvaro Pejenaute, Elena Ainzúa, Eduardo Ansorena, Gloria Abizanda, Felipe Prósper, Carlos de Miguel, Guillermo Zalba

{"title":"Endothelial NOX5 overexpression induces changes in the cardiac gene profile: potential impact in myocardial infarction?","authors":"Adriana Cortés, Javier Marqués, Álvaro Pejenaute, Elena Ainzúa, Eduardo Ansorena, Gloria Abizanda, Felipe Prósper, Carlos de Miguel, Guillermo Zalba","doi":"10.1007/s13105-023-00975-z","DOIUrl":"10.1007/s13105-023-00975-z","url":null,"abstract":"Cardiovascular diseases and the ischemic heart disease specifically constitute the main cause of death worldwide. The ischemic heart disease may lead to myocardial infarction, which in turn triggers numerous mechanisms and pathways involved in cardiac repair and remodeling. Our goal in the present study was to characterize the effect of the NADPH oxidase 5 (NOX5) endothelial expression in healthy and infarcted knock-in mice on diverse signaling pathways. The mechanisms studied in the heart of mice were the redox pathway, metalloproteinases and collagen pathway, signaling factors such as NFκB, AKT or Bcl-2, and adhesion molecules among others. Recent studies support that NOX5 expression in animal models can modify the environment and predisposes organ response to harmful stimuli prior to pathological processes. We found many alterations in the mRNA expression of components involved in cardiac fibrosis as collagen type I or TGF-β and in key players of cardiac apoptosis such as AKT, Bcl-2, or p53. In the heart of NOX5-expressing mice after chronic myocardial infarction, gene alterations were predominant in the redox pathway (NOX2, NOX4, p22phox, or SOD1), but we also found alterations in VCAM-1 and β-MHC expression. Our results suggest that NOX5 endothelial expression in mice preconditions the heart, and we propose that NOX5 has a cardioprotective role. The correlation studies performed between echocardiographic parameters and cardiac mRNA expression supported NOX5 protective action.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"787-797"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9965777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Construction of a hepatocytes-related and protein kinase-related gene signature in HCC based on ScRNA-Seq analysis and machine learning algorithm. 基于ScRNA-Seq分析和机器学习算法构建HCC肝细胞相关和蛋白激酶相关基因标记。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-11-01 Epub Date: 2023-07-17 DOI: 10.1007/s13105-023-00973-1

Zhuoer Zhang, Lisha Mou, Zuhui Pu, Xiaoduan Zhuang

{"title":"Construction of a hepatocytes-related and protein kinase-related gene signature in HCC based on ScRNA-Seq analysis and machine learning algorithm.","authors":"Zhuoer Zhang, Lisha Mou, Zuhui Pu, Xiaoduan Zhuang","doi":"10.1007/s13105-023-00973-1","DOIUrl":"10.1007/s13105-023-00973-1","url":null,"abstract":"With recent advancements in single-cell sequencing and machine learning methods, new insights into hepatocellular carcinoma (HCC) progression have been provided. Protein kinase-related genes (PKRGs) affect cell growth, differentiation, apoptosis, and signaling during HCC progression, making the predictive relevance of PKRGs in HCC highly necessary for personalized medicine. In this study, we analyzed single-cell data of HCC and used the machine learning method of LASSO regression to construct PKRG prediction models in six major cell types. CDK4 and AURKB were found to be the best PKRG prognostic signature for predicting the overall survival of HCC patients (including TCGA, ICGC, and GEO datasets) in hepatocytes. Independent clinical factors were further screened out using the COX regression method, and a nomogram combining PKRGs and cancer status was created. Treatment with Palbociclib (CDK4 Inhibitor) and Barasertib (AURKB Inhibitor) inhibited HCC cell migration. Patients classified as PKRG high- or low-risk groups showed different tumor mutation burdens, immune infiltrations, and gene enrichment. The PKRG high-risk group showed higher tumor mutation burdens and gene set enrichment analysis indicated that cell cycle, base excision repair, and RNA degradation pathways were more enriched in these patients. Additionally, the PKRG high-risk group demonstrated higher infiltration levels of Naïve CD8+ T cells, Endothelial cells, M2 macrophage, and Tregs than the low-risk group. In summary, this study established the hepatocytes-related PKRG signature for prognostic stratification at the single-cell level by using machine learning algorithms in HCC and identified potential HCC treatment targets based on the PKRG signature.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"771-785"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9826675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prognostication in NAFLD: physiological bases, clinical indicators, and newer biomarkers. NAFLD的预后:生理基础、临床指标和新的生物标志物。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2023-11-01 Epub Date: 2022-12-06 DOI: 10.1007/s13105-022-00934-0

Francesca Terracciani, Andrea Falcomatà, Paolo Gallo, Antonio Picardi, Umberto Vespasiani-Gentilucci

{"title":"Prognostication in NAFLD: physiological bases, clinical indicators, and newer biomarkers.","authors":"Francesca Terracciani, Andrea Falcomatà, Paolo Gallo, Antonio Picardi, Umberto Vespasiani-Gentilucci","doi":"10.1007/s13105-022-00934-0","DOIUrl":"10.1007/s13105-022-00934-0","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is becoming an epidemic in Western countries. Notably, while the majority of NAFLD patients will not evolve until advanced liver disease, a minority of them will progress towards liver-related events. Therefore, risk stratification and prognostication are emerging as fundamental in order to optimize human and economic resources for the care of these patients.Liver fibrosis has been clearly recognized as the main predictor of poor hepatic and extrahepatic outcomes. However, a prediction based only on the stage of fibrosis is near-sighted and static, as it does not capture the propensity of disease to further progress, the speed of progression and their changes over time. These determinants, which result from the interaction between genetic predisposition and acquired risk factors (obesity, diabetes, etc.), express themselves in disease activity, and can be synthesized by biomarkers of hepatic inflammation and fibrogenesis.In this review, we present the currently available clinical tools for risk stratification and prognostication in NAFLD specifically with respect to the risk of progression towards hard hepatic outcomes, i.e., liver-related events and death. We also discuss about the genetic and acquired drivers of disease progression, together with the physiopathological bases of their come into action. Finally, we introduce the most promising biomarkers in the direction of repeatedly assessing disease activity over time, mainly in response to future therapeutic interventions.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"851-868"},"PeriodicalIF":3.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35211238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3