General physiology and biophysics最新文献_第6页

Trivalent anions as probes of the CFTR channel pore. 作为 CFTR 通道孔探针的三价阴离子。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024007

Paul Linsdell

{"title":"Trivalent anions as probes of the CFTR channel pore.","authors":"Paul Linsdell","doi":"10.4149/gpb_2024007","DOIUrl":"10.4149/gpb_2024007","url":null,"abstract":"The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel uses positively charged amino-acid side-chains to form binding sites for permeating anions. These binding sites have been investigated experimentally using a number of anionic probes. Mutations that alter the distribution of positive and negative charges within the pore have differential effects on the binding of monovalent versus divalent anions. This study uses patch clamp recording from wild-type and pore-mutant forms of CFTR to investigate small trivalent anions (Co(NO2)63-, Co(CN)3- and IrCl63-) as potential probes of anion binding sites. These anions caused weak block of Cl- permeation in wild-type CFTR (Kd ≥ 700 μM) when applied to the intracellular side of the membrane. Mutations that increase the density of positive charge within the pore (E92Q, I344K, S1141K) increased the binding affinity of these anions 80-280-fold, and also greatly increased the voltage-dependence of block, consistent with fixed charges in the pore affecting monovalent : multivalent anion selectivity. However, high-affinity pore block by Co(NO2)63-apparently did not alter channel gating, a hallmark of high-affinity binding of divalent Pt(NO2)42- ions within the pore. This work increases the arsenal of probes available to investigate anion binding sites within Cl- channel pores.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 3","pages":"197-207"},"PeriodicalIF":1.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Daidzein protects endothelial cells against high glucose-induced injury through the dual-activation of PPARα and PPARγ. 通过 PPARα 和 PPARγ 的双重激活，Daidzein 可保护内皮细胞免受高血糖诱导的损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023041

Xuemei Yang, Xinhui Jiang, Changqing Liu, Chuang Yang, Sheng Yao, Hongmei Qiu, Junxia Yang, Ke Wu, Hong Liao, Qingsong Jiang

{"title":"Daidzein protects endothelial cells against high glucose-induced injury through the dual-activation of PPARα and PPARγ.","authors":"Xuemei Yang, Xinhui Jiang, Changqing Liu, Chuang Yang, Sheng Yao, Hongmei Qiu, Junxia Yang, Ke Wu, Hong Liao, Qingsong Jiang","doi":"10.4149/gpb_2023041","DOIUrl":"10.4149/gpb_2023041","url":null,"abstract":"Endothelial damage caused by persistent glucose and lipid metabolism disorders is the main reason of diabetic vascular diseases. Daidzein exerts positive effects on vascular dysfunction. Peroxisome proliferator-activated receptors (PPARs) regulate critically glucose and lipid metabolism. However, the interaction of daidzein to PPARs is still insufficiently explored. In this study, the cell proliferation was detected by EdU. The intrinsic activity and binding affinity of daidzein for human PPARs (hPPARs) were estimated by transactivation reporter gene test and HPLC-UV method, respectively. Daidzein significantly reversed high glucose (HG, at 30 mmol/l)-induced injury in HUVECs, which was inhibited by both PPARα and PPARγ antagonist, but no PPARβ antagonist. Daidzein selectively activated hPPARα and hPPARγ1, but weakly hPPARβ. Additionally, daidzein also bound to both hPPARα and hPPARγ1. The findings suggested that daidzein may be a PPARα and PPARγ dual-agonist. The amelioration of daidzein on HUVECs from hyperglycemia may be mediated by the activation of PPARα and PPARγ receptors.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"153-162"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

TRIM67 interacts with ENAH to regulate the apoptosis and autophagy of lung cancer cells. TRIM67 与ENAH相互作用，调节肺癌细胞的凋亡和自噬。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023037

Rui Liu, Kun Miao, Ling Gao, Ling He

引用次数: 0

The role of endoplasmic reticulum stress-related genes in the diagnosis and subtyping of non-alcoholic fatty liver disease. 内质网应激相关基因在非酒精性脂肪肝的诊断和亚型分类中的作用。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023042

Zihao Guo, Xiaoxiao Yu, Zhihao Fang, Kai Yang, Changxu Liu, Zhichao Dong, Chang Liu

{"title":"The role of endoplasmic reticulum stress-related genes in the diagnosis and subtyping of non-alcoholic fatty liver disease.","authors":"Zihao Guo, Xiaoxiao Yu, Zhihao Fang, Kai Yang, Changxu Liu, Zhichao Dong, Chang Liu","doi":"10.4149/gpb_2023042","DOIUrl":"10.4149/gpb_2023042","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide. Chronic activation of endoplasmic reticulum stress (ERS) in hepatocytes may promote the development of NAFLD, yet endoplasmic reticulum stress-related genes (ERSGs) have not been studied in NAFLD. Our aim is to study the relationship between ERSGs and the immune microenvironment of NAFLD patients and to construct predictive models. We screened 48 endoplasmic reticulum stress-related differentially expressed genes (ERSR-DEGs) using data from two GEO datasets and the GeneCards database. Enrichment analysis revealed that ERSR-DEGs are closely associated with immune-related pathways and functions. The immune infiltration profile of NAFLD was obtained by single sample gene set enrichment analysis (ssGSEA). There were significant differences in immune cell infiltration and immune function between NAFLD group and control group. Using 113 NAFLD samples, we explored two molecular clusters based on ERSR-DEGs. A five-gene SVM model was selected as the best machine learning model, and a nomogram based on five-gene SVM model showed good predictive efficiency. The mRNA expression levels of POR, PPP1R15A, FOS and FAS were significantly different between NAFLD mice and healthy mice. In conclusion, ERS is closely associated with the development of NAFLD. We established a promising and SVM-based predictive model to assess the risk of disease in patients with ERS subtypes and NAFLD.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"85-102"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Network pharmacology and pharmacological evaluation of Wenzheng Jiedu Powder Modified Formula for neuropathic pain relief. 缓解神经病理性疼痛的文正街杜粉改良方的网络药理学和药效学评价

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023040

Yanping Li, Feng Yang, Wanying Lang, Qi An, Zhi Pan, Wenyu Shi, Xiaowei Shi

{"title":"Network pharmacology and pharmacological evaluation of Wenzheng Jiedu Powder Modified Formula for neuropathic pain relief.","authors":"Yanping Li, Feng Yang, Wanying Lang, Qi An, Zhi Pan, Wenyu Shi, Xiaowei Shi","doi":"10.4149/gpb_2023040","DOIUrl":"10.4149/gpb_2023040","url":null,"abstract":"This study aimed to elucidate the mechanism of Wenzheng Jiedu Powder Modified Formula (WJPMF) in treating neuropathic pain (NP). Network pharmacology and experimental verification were integrated to explore the therapeutic effects and key targets of WJPMF. Active components, corresponding target genes, and absorption, distribution, metabolism, and excretion (ADME) genes of WJPMF against NP were screened from public databases. Network analysis and molecular docking were conducted to identify key targets and verify binding abilities. In vivo experiments were performed on spared nerve injury (SNI) rats to assess the analgesic effects and regulatory mechanisms of WJPMF. WJPMF significantly improved pain behaviors in SNI rats by regulating ATP-binding cassette transporter A1 (ABCA1), peroxisome proliferator-activated receptor alpha (PPARA), peroxisome proliferator-activated receptor gamma (PPARG), and superoxide dismutase 2 (SOD2) expression, which were key targets involved in the peroxisome proliferator-activated receptor (PPAR) signaling pathway. WJPMF shows promising therapeutic potential for NP through the modulation of specific targets, offering a novel therapeutic strategy for managing NP.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"139-152"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

miR-497-5p promoted neuronal injury in ischemic stroke by inhibiting the BDNF/TrkB/PI3K/Akt pathway. miR-497-5p 通过抑制 BDNF/TrkB/PI3K/Akt 通路促进缺血性中风的神经元损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023038

Chunyan Gong, Xiaona He, Guiliang Li, Dayu Wang, Yonghua Yang, Yanping Shi, Wenbing Su, Yuanxian Wu

{"title":"miR-497-5p promoted neuronal injury in ischemic stroke by inhibiting the BDNF/TrkB/PI3K/Akt pathway.","authors":"Chunyan Gong, Xiaona He, Guiliang Li, Dayu Wang, Yonghua Yang, Yanping Shi, Wenbing Su, Yuanxian Wu","doi":"10.4149/gpb_2023038","DOIUrl":"10.4149/gpb_2023038","url":null,"abstract":"The aim of this study was to investigate the molecular mechanism by which miR-497-5p regulates neuronal injury after ischemic stroke through the BDNF/TrkB/Akt signaling pathway. PC12 cells were used to construct a stroke injury model by oxygen-glucose deprivation/reoxygenation (OGD/R). The expression level of miR-497-5p was measured by RT-qPCR. CCK-8 kit was used to detect cell viability. Cell apoptosis and reactive oxygen species (ROS) were detected by flow cytometry. MDA and SOD detection kits were used to detect MDA content and SOD activity. A double luciferase reporter system was used to verify the targeting relationship between miR-497-5p and BDNF. The expression of BDNF, TrkB, p-TrkB, Akt and p-Akt was detected by Western blot. We have found that miR-497-5p expression was inhibited after treatment with OGD/R. Simultaneously, cell apoptosis, MDA content and ROS were upregulated, while cell viability and SOD were significantly decreased in PC12 cells. The effects of OGD/R on PC12 cells were reversed with the downregulation of miR-497-5p. A double luciferase reporter assay demonstrated that miR-497-5p negatively targets BDNF. BDNF inhibited cell apoptosis and oxidative stress injury in PC12 cells. These findings suggest that miR-497-5p aggravates neuronal injury in experimental model of ischemic stroke by inhibiting the BDNF/TrkB/PI3K/Akt signaling pathway.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"175-183"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Mobile telephony radiation exerts genotoxic action and significantly enhances the effects of gamma radiation in human cells. 移动电话辐射会产生基因毒性作用，并明显增强伽马辐射对人体细胞的影响。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 Epub Date: 2023-12-08 DOI: 10.4149/gpb_2023036

Dimitris J Panagopoulos

{"title":"Mobile telephony radiation exerts genotoxic action and significantly enhances the effects of gamma radiation in human cells.","authors":"Dimitris J Panagopoulos","doi":"10.4149/gpb_2023036","DOIUrl":"10.4149/gpb_2023036","url":null,"abstract":"I previously reported chromosomal damage in human peripheral blood lymphocytes (HPBLs) induced by: a) mobile telephony (MT) electromagnetic fields (EMFs)/electromagnetic radiation (EMR), b) a high caffeine dose, and c) the combination of the two stressors. HPBLs from the same subjects exposed to gamma radiation at doses 0.1, 0.3, or 0.5 Gy, displayed more aberrations than those exposed to MT EMFs or the high caffeine dose in a dose-dependent manner. When the cells exposed to these gamma radiation doses were pre-exposed to a single 15-min MT EMF exposure, the number of aberrations increased significantly more than the sum number of aberrations induced by the individual stressors in all subjects. Thus, MT EMF exposure at a power density ~136 times below the latest International Commission on Non- Ionizing Radiation Protection (ICNIRP) exposure limit, apart from the fact that it is genotoxic by itself, significantly enhanced the genotoxic action of gamma radiation. Since gamma radiation at similar doses is applied for diagnostic and therapeutic purposes, people should be aware of the increased risk during treatment periods. Comparison of the genotoxic action between MT EMF and gamma radiation shows that the ICNIRP limits are, at least, ~4.5×104 times less stringent than the limits for gamma radiation.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":" ","pages":"103-120"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138801398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

ANGPT1 promotes M1 macrophage polarization and inhibits lung adenocarcinoma progression by inhibiting the TGF-β signalling pathway. ANGPT1 通过抑制 TGF-β 信号通路促进 M1 巨噬细胞极化并抑制肺腺癌的进展。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2024001

Gang Liu, Hao Zhang

{"title":"ANGPT1 promotes M1 macrophage polarization and inhibits lung adenocarcinoma progression by inhibiting the TGF-β signalling pathway.","authors":"Gang Liu, Hao Zhang","doi":"10.4149/gpb_2024001","DOIUrl":"10.4149/gpb_2024001","url":null,"abstract":"Immune cells in the immune microenvironment of lung adenocarcinoma (LUAD) are involved in tumour progression. The aim of this study was to investigate the molecular mechanisms of immune infiltration-related genes in LUAD. The GEO, GeneCards, BioGPS and Genehopper databases were utilized to screen for immune infiltration-related differentially expressed genes (DEGs) in LUAD. Protein-protein interaction (PPI) network construction and survival analysis were performed in the Kaplan-Meier database to identify hub genes. The TIMER 2.0 database was used to analyse the correlations between hub gene expression and immune infiltration level. Co-culture of LUAD cells with macrophages and plasmid transfection to overexpress ANGPT1 were performed to investigate the function of the hub genes in LUAD using RT-qPCR, Western blot, CCK-8 assays, cell wound healing assays and transwell assays. A total of 88 immune infiltration-related DEGs were screened. The hub genes ANGPT1, CDH5 and CLDN5 were reduced in LUAD, while COL3A1 was overexpressed. ANGPT1 was significantly correlated with OS, FP and PPS, and ANGPT1 promoted the polarization of M1 macrophages. Further experiments revealed that ANGPT1 inhibited the proliferation, migration and invasion of LUAD cells by inhibiting the TGF-β signalling pathway. ANGPT1 promotes polarization of M1 macrophages and reduces the progression of LUAD by inhibiting the TGF-β signalling pathway. Thus, ANGPT1 could be employed as a predictive biomarker and immunotherapy target for lung cancer.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 2","pages":"121-138"},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Effect of quercetin administration during the first two weeks post-weaning on the development of non-alcoholic fatty liver disease and dyslipidaemia in Sprague Dawley rats fed a high fructose diet. 断奶后头两周服用槲皮素对以高果糖为食的 Sprague Dawley 大鼠非酒精性脂肪肝和血脂异常的发展有何影响？

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-01-01 DOI: 10.4149/gpb_2023033

Ramatsobane Tladi, Kennedy H Erlwanger, Janine Donaldson

{"title":"Effect of quercetin administration during the first two weeks post-weaning on the development of non-alcoholic fatty liver disease and dyslipidaemia in Sprague Dawley rats fed a high fructose diet.","authors":"Ramatsobane Tladi, Kennedy H Erlwanger, Janine Donaldson","doi":"10.4149/gpb_2023033","DOIUrl":"10.4149/gpb_2023033","url":null,"abstract":"Hepatic steatosis and dyslipidaemia are associated with excessive fructose consumption. We investigated the effect of quercetin intake during the early pre-weaning period on metabolic dysfunction caused by a high fructose diet. Sprague Dawley rats, 21-day-old, were weaned onto standard rat chow and randomly allocated to four groups which either water or 20% fructose solution to drink with or without quercetin (100 mg/kg body mass). Quercetin was administered for two weeks. Thereafter, rats continued on their respective diets for six weeks without quercetin. Terminally, serum triglyceride concentrations were not significantly different (p > 0.05) between males across groups. However, females receiving quercetin alone had lower serum triglyceride levels than those receiving fructose (p < 0.01). Quercetin increased the incidence of hepatic steatosis in female rats. Quercetin intake in the immediate post-weaning period may prevent hypertriglyceridemia. However, female rats receiving quercetin alone are predisposed to hepatic steatosis associated with a high fructose diet.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 1","pages":"25-36"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139680985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Inactivation of the TGF-β1/ALK5 axis enhances club cell function and alleviates lung tissue damage to ameliorate COPD progression through the MEK/ERK signaling pathway. TGF-β1/ALK5轴失活可增强俱乐部细胞功能，减轻肺组织损伤，从而通过MEK/ERK信号通路改善慢性阻塞性肺病的进展。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-01-01 DOI: 10.4149/gpb_2023034

Jing Tian, Hui Ouyang, Jie Wu, Lu Wen, Xiaoping Li, Fangying Yang, Hao Yuan

{"title":"Inactivation of the TGF-β1/ALK5 axis enhances club cell function and alleviates lung tissue damage to ameliorate COPD progression through the MEK/ERK signaling pathway.","authors":"Jing Tian, Hui Ouyang, Jie Wu, Lu Wen, Xiaoping Li, Fangying Yang, Hao Yuan","doi":"10.4149/gpb_2023034","DOIUrl":"10.4149/gpb_2023034","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is a highly prevalent and fatal disease worldwide. The function of club cells, which are considered progenitor/stem cells of the bronchial epithelium, and their secreted protein CC16, have been proposed as potential targets for COPD treatment. This study aimed to investigate the role of the TGF-β1/ALK5 signaling pathway in club cell function and COPD progression. C57BL/6J mice were divided into Normal group (exposed to fresh air) and COPD group (exposed to incremental cigarette smoke extract for 12 weeks). The COPD mice were further divided into COPD group, DMSO group, and LY2109761 group (injected with 150 mg/kg LY2109761, a TGF-β1 inhibitor). Tissue staining was used to assess lung damage, and the expression of CC16 was measured. The levels of inflammatory factors and DNA damage-related indicators were also measured. The involvement of the MEK/ERK signaling pathway was determined. COPD mice exhibited severe lung damage and impaired club cell function. Activation of the TGF-β1/ALK5 and MEK/ERK pathways were observed in COPD mice. However, administration of LY2109761 in COPD mice inactivated the TGF-β1/ALK5 and MEK/ERK pathways. Administration of LY2109761 also alleviated pulmonary fibrosis, downregulated the levels cleaved caspase-3, IL-4, IL-5, IL-13, IL-12, and IFN-γ, and limited the phosphorylation of Chk1. Moreover, LY2109761 enhanced CC16 expression and decreased lung cell apoptosis. Inactivation of the TGF-β1/ALK5 axis inhibits the MEK/ERK signaling pathway, enhances club cell function, and alleviates lung tissue damage. These findings suggest that TGF-β1 is a potential therapeutic target for COPD.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"43 1","pages":"37-48"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139680987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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