JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
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2024
·Vol. 28
·期 20
·e70144
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IF 4.3
Qiying Yao,Xinrui Hu,Tiantian Bian,Qing Zhang,Zhao Xue,Yuesheng Lv,Shupeng Ren,Yue Chen,Dongmei Zhang,Liang Chen
Sialylation catalysed by sialyltransferase 7A (SIAT7A) plays a role in the development of cardiac hypertrophy. However, the regulatory mechanisms upstream of SIAT7A in this context remain poorly elucidated. Previous study demonstrated that KLF4 activates the SIAT7A gene in ischemic myocardium by binding to its promoter region. Nevertheless, the potential involvement of KLF4 in regulating SIAT7A expression in Ang II-induced hypertrophic cardiomyocytes remains uncertain. This study seeks to deepen the underlying mechanisms of the KLF4 and SIAT7A interaction in the progression of Ang II-induced cardiac hypertrophy. The results showed a concurrent increase in SIAT7A and KLF4 levels in hypertrophic myocardium of essential hypertension patients and in hypertrophic cardiomyocytes stimulated by Ang II. In vitro experiments revealed that reducing KLF4 levels led to a decrease in both SIAT7A synthesis and Sialyl-Tn antigen expression, consequently inhibiting Ang II-induced cardiomyocyte hypertrophy. Intriguingly, reducing SIAT7A levels also resulted in decreased KLF4 expression and suppression cardiomyocyte hypertrophy. Consistent with this, elevating SIAT7A levels increased KLF4 expression and exacerbated cardiomyocyte hypertrophy in both in vivo and in vitro experiments. Additionally, a time-course analysis indicated that KLF4 expression preceded that of SIAT7A. Luciferase reporter assays further confirmed that modulating SIAT7A levels directly influenced the transcriptional activity of KLF4 in cardiomyocytes. In summary, KLF4 expression is upregulated in cardiomyocytes treated with Ang II, which subsequently induces the expression of SIAT7A. The elevated levels of SIAT7A, in turn, enhance the transcription of KLF4 . These findings suggest a positive feedback loop between KLF4 and SIAT7A-Sialyl-Tn, ultimately promoting Ang II-induced cardiac hypertrophy.
研究领域:
心脏病学
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分子生物学
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细胞生物学
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DOI
高影响因子
Food Science and Human Wellness
·
2024
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IF 5.6
Xianghui Huang,Jia Xu,Ye Xu,Bingxin Huangfu,Feng Zhang,Yanzhou Hu,Ruxin Gao,Xinxin Ren,Boyang Zhang,Kunlun Huang,Xiaoyun He
Non-alcoholic fatty liver disease (NAFLD) has become a global issue and a severe threat to public health. However, to date, no approved therapeutic drugs have been developed. Dietary interventions with natural products have shown promise in preventing and treating NAFLD. Sulforaphane (SFN) is a phytocompound with antioxidant and anti-inflammatory properties, and previous research has demonstrated that SFN can ameliorate hepatic lipid accumulation and inflammation. However, the molecular mechanisms underlying these beneficial effects remain unclear. In this study, we confirmed the protective effects of SFN on excessive lipid accumulation and inflammatory injury in a high-fat, high-fructose diet-induced non-alcoholic steatohepatitis (NASH) mouse model. We found that SFN attenuates the inflammatory injury in a macrophage cell line and the liver of NASH mice, owing to the promotion of M1-type macrophage polarization toward the M2-type and the regulation of inflammatory mediators. Further analysis demonstrated that this SFN-induced macrophage M2-type polarization occurs in a Krüppel-like factor 4 (KLF4)-dependent manner. In summary, we uncovered a new mechanism of action underlying SFN activity and provide evidence that dietary intervention with SFN might be protective against NASH.
研究领域:
肝病学
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免疫学
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药理学
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营养学
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DOI
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·1-16
·
IF 3.9
Feng Wenguang,Wang Haibin,Zhang Guoliang,Gao Wang,LI Hongcang,Liu Haibo,Sun Yanhong
Objective To explore the role and mechanism of transcription factor KLF4 in regulating mitochondrial damage and apoptosis by activating chondrocyte autophagy. Human primary chondrocytes were treated with IL-1β to establish an in vitro osteoarthritis model. KLF4 was overexpressed using lentivirus to intervene in chondrocytes. Cell apoptosis and mitochondrial membrane potential were detected by flow cytometry. Mitochondrial morphology was observed under transmission electron microscopy. Cell ATP level was detected by ELISA. Ca2 + homeostasis was detected by flow cytometry with Fluo-3/AM fluorescence labeling. The expression of autophagy-related proteins Beclin1, P62, and LC3 was detected by WB. The interaction between transcription factor KLF4 and gene p62 promoter was verified by dual luciferase assay. The interaction between p62, Beclin1 and KLF4 was verified by Chip assay. To further explore the relationship between KLF4 and autophagy, KLF4 was overexpressed and treated with autophagy inhibitor 3-MA (5mmol/L). The expression of autophagy-related proteins Beclin1, P62, and LC3 was detected by WB. Cell apoptosis level was detected by flow cytometry. The mitochondrial membrane potential level was detected by flow cytometry. Ca2 + homeostasis was detected by flow cytometry with Fluo-3/AM fluorescence labeling. In chondrocytes treated with IL-1β, TNF-α levels increased significantly, apoptosis rate rose, and ATP generation declined. However, after overexpression of KLF4, apoptosis level decreased significantly; ATP level increased significantly, and mitochondrial structure and function gradually recovered. Flow cytometry detection of mitochondrial membrane potential showed a significant decrease after KLF4 overexpression, and Ca2 + homeostasis was partially restored. WB detection of autophagy-related proteins showed a significant increase in p62 and cellular autophagy levels. Dual luciferase results indicated that transcription factor KLF4 interacted with the promoter of gene p62; Chip experiment results suggested that KLF4 may interact with the promoter regions of P62 and Beclin1. After KLF4 overexpression combined with 3-MA treatment, compared with empty load combined with 3-MA, p62 and LC3 protein expression increased significantly, apoptosis level decreased significantly, and membrane potential level decreased. Transcription factor KLF4 can regulate mitochondrial damage and apoptosis by activating chondrocyte autophagy.
研究领域:
分子生物学
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风湿病学
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细胞生物学
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转化医学
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骨骼疾病
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信号转导
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基因调控
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线粒体功能
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产品关联
DOI
PubMed
高影响因子
Experimental and Therapeutic Medicine
·
2021
·Vol. 22
·期 3
·1-10
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IF 2.447
Jing Li,Yu-Shan Mao,Fen Chen,Dong-Xia Xia,Tin-Qi Zhao
Insulin resistance is the main sign of type 2 diabetes mellitus and is often accompanied by the infiltration of inflammatory factors. These inflammatory factors are mainly produced and secreted by macrophages. The purpose of the current study was to explore the relationship between macrophages and insulin resistance, and to determine its underlying mechanism. The insulin resistance of macrophages was induced by palmitic acid (PA) in vitro. The glucose uptake rate of macrophages, the expression levels of inflammatory cytokines and the expression levels of insulin resistance‑related proteins were detected. The protein expression levels of Krüppel‑like factor 4 (KLF4), toll‑like receptor 4 (TLR4), NF‑κB and Galectin‑3 (Gal‑3) were detected via western blotting and recovery experiments were performed by combining the Gal‑3 and TLR4 inhibitors GB1107 and TAK242. The results revealed that PA‑induced macrophages demonstrated insulin resistance. Additionally, KLF4 protein was inhibited and the sugar uptake rate was significantly lower than that of the control group. Western blotting and immunofluorescence assays revealed that the expression of Gal‑3 in PA‑induced macrophages was significantly upregulated. The addition of the Gal‑3 inhibitor GB1107 significantly increased glucose utilization and reduced insulin resistance in PA‑treated cells. Inhibitor of TLR4 inhibited the protein expression level of the TLR4/NF‑κB pathway. In conclusion, PA promoted the TLR4/phosphorylated‑NF‑κB signaling pathway by inhibiting KLF4, promoted the upregulation of Gal‑3 expression and improved the insulin resistance of macrophages.
研究领域:
免疫学
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内分泌学
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分子生物学
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糖尿病研究
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DOI
PubMed
高影响因子
CELLULAR SIGNALLING
·
2023
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IF 4.8
Zeyu Xing,Mingyang Du,Yanhua Zhen,Jie Chen,Dongdong Li,Ruyin Liu,Jiahe Zheng
Atherosclerosis (AS), a metabolic disorder , is usually caused by chronic inflammation. LETM1 Domain-Containing Protein 1 (LETMD1) is a mitochondrial outer membrane protein required for mitochondrial structure. This study aims to evaluate the functional role of LETMD1 in endothelial pathogenesis of AS. Oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) and high-fat diet apolipoprotein E -deficient (ApoE −/− ) mice were used to establish in vitro and in vivo models, respectively. Recombinant adenovirus vectors were constructed to investigate the role of LETMD1 in AS. mRNA sequencing was used to explore the effect of LETMD1 overexpression on gene expression in ox-LDL-induced HUVECs. A dual-luciferase reporting assay and chromatin immunoprecipitation (ChIP)-PCR were further conducted to verify the relationship between KLF4 and LETMD1. Results showed that LETMD1 was highly expressed in the aortas of atherosclerotic animals. LETMD1 overexpression reduced the expression of inflammatory factors, pyroptosis , ROS production, and NF-κB activation in ox-LDL-induced HUVECs, whereas LETMD1 knockdown had the opposite impact. LETMD1 overexpression was involved in regulating gene expression in ox-LDL-induced HUVECs. Overexpression of LETMD1 in mice reduced serum lipid levels as well as atherosclerotic lesions in the aortic roots. Furthermore, LETMD1 overexpression suppressed inflammatory reactions, cell pyroptosis, nuclear p65 protein level, cell apoptosis, and ROS generation in the aortas of AS mice. KLF4 (Krüppel-like factor 4) was found to be the transcriptional regulator of LETMD1. In conclusion, LETMD1, a target of KLF4, hinders endothelial inflammation and pyroptosis, which is a mechanism inhibiting the development of atherosclerosis.
研究领域:
心血管疾病
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分子生物学
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细胞生物学
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炎症
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转录调控
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DOI
PubMed
高影响因子
MOLECULAR MEDICINE
·
2023
·Vol. 29
·期 1
·1-19
·
IF 5.7
Han Zhiyang,Hu Haidi,Yin MingZhu,Lin Yu,Yan Yan,Han Peng,Liu Bing,Jing Bao
Background Macrophage-like transformation of vascular smooth muscle cells (VSMCs) is a risk factor of atherosclerosis (AS) progression. Transcription factor homeobox A1 (HOXA1) plays functional roles in differentiation and development. This study aims to explore the role of HOXA1 in VSMC transformation, thereby providing evidence for the potential mechanism of AS pathogenesis.Methods High fat diet (HFD)-fed apolipoprotein E knockout (ApoE−/−) mice were applied as an in vivo model to imitate AS, while 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POV-PC)-treated VSMCs were applied as an in vitro model. Recombinant adeno-associated-virus-1 (AAV-1) vectors that express short-hairpin RNAs targeting HOXA1, herein referred as AAV1-shHOXA1, were generated for the loss-of-function experiments throughout the study.Results In the aortic root of AS mice, lipid deposition was severer and HOXA1 expression was higher than the wide-type mice fed with normal diet or HFD. Silencing of HOXA1 inhibited the AS-induced weight gain, inflammatory response, serum and liver lipid metabolism disorder and atherosclerotic plaque formation. Besides, lesions from AS mice with HOXA1 knockdown showed less trans-differentiation of VSMCs to macrophage-like cells, along with a suppression of krüppel-like factor 4 (KLF4) and nuclear factor (NF)-κB RelA (p65) expression. In vitro experiments consistently confirmed that HOXA1 knockdown suppressed lipid accumulation, VSMC-to-macrophage phenotypic switch and inflammation in POV-PC-treated VSMCs. Mechanism investigations further illustrated that HOXA1 transcriptionally activated RelA and KLF4 to participate in the pathological manifestations of VSMCs.Conclusion sHOXA1 participates in AS progression by regulating VSMCs plasticity via regulation of NF-κB p65 and KLF4. HOXA1 has the potential to be a biomarker or therapeutic target for AS.
研究领域:
心血管疾病
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分子生物学
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病理学
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DOI
PubMed
高影响因子
Molecular Medicine Reports
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2021
·Vol. 24
·期 4
·1-7
·
IF 2.952
Yongpan Huang,Xiaodong Han,Jiayu Tang,Xian Long,Xiaoye Wang
Homocysteine (Hcy) was discovered to be an independent risk factor for the development of atherosclerosis (AS). Moreover, endothelial‑mesenchymal transition (EndMT) was found to be one of main mechanisms contributing to the pathogenesis of AS. Salidroside (SAL) has diverse pharmacological activities, including anti‑inflammatory, anti‑cancer, anti‑oxidative and anti‑fibrosis properties. However, whether SAL serves a beneficial role in Hcy‑induced EndMT remains unknown. The present study aimed to investigate whether SAL exerted its effects on Hcy‑induced EndMT via the Kruppel‑like factor 4 (KLF4)/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway. HUVECs were pretreated with high and low doses (10 or 50 µmol/l) of SAL for 2 h, followed by 1 mmol/l Hcy for 48 h to induce EndMT. Western blotting was used to analyze the protein expression levels of the endothelial marker, VE‑cadherin, the mesenchymal cell marker, α‑smooth muscle actin (SMA), and the nuclear transcription factors, KLF4 and eNOS. Wound healing assays were used to determine the cell migratory ability, and the levels of NO in the cell culture supernatants were measured using a nitrate reductase assay. Cellular immunofluorescence was used to analyze the expression and localization of KLF4. Small interfering (si)RNA targeting KLF4 (siKLF4) was used to knock down KLF4 expression in HUVECs. The results of the present study revealed that treatment with SAL upregulated the expression levels of VE‑cadherin, downregulated the expression levels of α‑SMA, reduced cell migration and activated the eNOS/NO signaling axis, as well as downregulated KLF4 expression and translocation to the nucleus. Compared with the SAL + siKLF4 co‑administration group, no significant differences were observed in the expression levels of the phenotypic markers in the SAL or siKLF4 groups. In conclusion, the findings of the present study revealed that SAL may inhibit Hcy‑induced EndMT via regulation of the KLF4/eNOS signaling pathway.
研究领域:
心血管疾病
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分子生物学
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药理学
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DOI
PubMed
高影响因子
CARDIOVASCULAR DRUGS AND THERAPY
·
2026
·
IF 3.5
Chen XinJing,Hong Jingxuan
Objective This study aimed to determine whether dexmedetomidine (DEX) attenuates myocardial ischemia/reperfusion injury (MIRI) by regulating DNA methyltransferase 3B (DNMT3B)–mediated methylation of a CpG island within the Kruppel-like factor 4 (KLF4) promoter. Methods A rat model of MIRI was established and treated with DEX, DNMT3B knockdown, or DEX combined with DNMT3B overexpression. Histopathological alterations, apoptosis, and DNMT3B/KLF4 expression were assessed using H&E staining, TUNEL/cTnT co-staining, RT-qPCR, western blot, immunofluorescence, and immunohistochemistry. H9C2 cardiomyocytes subjected to oxygen-glucose deprivation/reperfusion (OGD/R) were treated with DEX and transfected with DNMT3B or KLF4 knockdown/overexpression plasmids. CpG island methylation within the KLF4 promoter was predicted using MSP and ChIP-PCR. Results MIRI impaired cardiac function, increased infarct size and myocardial enzyme release, upregulated DNMT3B expression, downregulated KLF4 expression, and promoted cardiomyocyte apoptosis. DNMT3B was predominantly localized in cTnT-positive cardiomyocytes. DEX treatment or DNMT3B knockdown reduced DNMT3B expression, restored KLF4 levels, and alleviated myocardial injury in vivo as well as OGD/R-induced damage in vitro . DEX was associated with decreased methylation of the investigated CpG island within the KLF4 promoter. DEX may inhibit DNMT3B-mediated promoter hypermethylation, thereby enhancing KLF4 transcription. KLF4 knockdown abolished the cardioprotective effects of DEX, while DNMT3B overexpression reversed DEX-mediated improvements in vivo . Conclusions DEX may attenuate MI/RI by downregulating DNMT3B and reducing methylation at a CpG island within the KLF4 promoter, thereby promoting KLF4 expression. However, the intrinsic resolution limitations of MSP and ChIP-PCR restrict precise mapping of methylation sites. Higher-resolution techniques, such as whole-genome bisulfite sequencing or single-molecule methylation sequencing, are warranted to validate these findings.
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高影响因子
Pigment Cell & Melanoma Research
·
2025
·Vol. 38
·期 4
·e70034
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IF 2.6
Man Cai,Liangyu Wang,Miao Sun,Meixi Liu,Yingchun Liu
Protein arginine methyltransferase 6 (PRMT6), a member of the PRMT family capable of self-arginine methylation, is down-regulated in melanoma, but the specific mechanism is still unclear. Our work demonstrated that PRMT6 overexpression significantly inhibited the ability of melanoma cells to proliferate, tumorigenicity, migration, and invasion, whereas PRMT6 knockdown rescued these malignant behaviors of melanoma cells. Mechanistically, we identified aldehyde dehydrogenase 1A1 (ALDH1A1) as a critical downstream target of PRMT6. PRMT6 knockdown up-regulated ALDH1A1 expression, exacerbating melanoma aggressiveness in vitro. Further investigations revealed that PRMT6 modulates ALDH1A1 expression by catalyzing asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) and antagonizing the enrichment of histone H3 lysine 4 trimethylation (H3K4me3) at the ALDH1A1 promoter. In addition, dual-luciferase experiments showed that the transcription factor KLF4 may bind to the −1800 ~ +45 sequence of PRMT6, thereby negatively regulating PRMT6 expression in melanoma. Our findings underscore the tumor-suppressive role of PRMT6 in melanoma pathogenesis, highlighting its potential as a novel therapeutic target, particularly for metastatic melanoma.
研究领域:
癌症生物学
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分子生物学
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表观遗传学
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生物化学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL DENTAL JOURNAL
·
2026
·Vol. 76
·期 4
·109587
·
IF 5.2
Jingkun Zhang,Li Lin,Huixian Dong,Bingtao Wang,Xiaoshi Chen,Chenhao Wang,Liecong Lin,Jialin Zhong,Guocong Zheng,Qianzhou Jiang
Background The regeneration of functional dentin is a critical clinical goal for preserving tooth vitality after injury, with odontoblastic differentiation of human dental pulp stem cells (hDPSCs) being central to this reparative process. While the long noncoding RNA H19 is recognised as a key regulator of dentin repair, its downstream regulatory network is complex and incompletely mapped. Beyond the previously established H19/miR-140-5p/BMP2 axis, this study identifies a distinct and parallel pathway in which H19 promotes odontoblastic differentiation by downregulating miR-103a-3p, which in turn targets the PIK3R1/AKT and KLF4 signalling cascades. Our findings reveal that these two downstream networks operate independently, further elucidating the multifaceted role of H19 in dentin regeneration. Methodology In this study, we used lentiviral vectors to stably overexpress H19 in hDPSCs. Bioinformatic analysis and dual-luciferase reporter assays were employed to validate the interactions between H19 and miR-103a-3p, as well as between miR-103a-3p and its target mRNAs, including phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) and Kruppel-like factor 4 (KLF4). And qPCR and Western blot were used to investigate the expression pattern of H19 and the potential signalling axis of H19 and key odontogenic markers. Then, alkaline phosphatase and alizarin red S staining were used to evaluate odontogenic differentiation capacity. Finally, a heterotopic pulp regeneration model was established. And HE staining, Masson staining, immunofluorescence and immunohistochemistry were performed to verify the mechanism of H19 regulating odontogenic differentiation in vivo. Results In vitro , H19 promoted odontogenic differentiation of hDPSCs, while miR-103a-3p inhibited them. Both PIK3R1 and KLF4 were identified as direct targets of miR-103a-3p. Ectopic expression of either PIK3R1 or KLF4 restored the odontogenic differentiation capacity of hDPSCs suppressed by miR-103a-3p. Mechanistically, PIK3R1 promoted odontogenesis by activating the PI3K/AKT signalling pathway, whereas KLF4 acted independently as a transcriptional regulator. In vivo , H19 overexpression drove odontoblastic differentiation of hDPSCs by inducing the expression of its downstream targets, PIK3R1 and KLF4. Conclusion Our findings indicated that H19 promoted odontogenic differentiation of hDPSCs by modulating the miR-103a-3p–PIK3R1/AKT and miR-103a-3p–KLF4 axes, underscoring their therapeutic potential for pulp regeneration.
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DOI
PubMed
高影响因子
Journal of Diabetes and Metabolic Disorders
·
2026
·Vol. 25
·期 1
·142
·
IF 2.1
Zhang Li,Zhang Chuanqi,Liu Yueyan,Zhang Chenchen
Background Atherosclerosis (AS) remains a major cause of cardiovascular morbidity and mortality worldwide. and Phenotypic switching of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic phenotype is a critical event in atherosclerotic lesion development. Although miR-148b has been implicated in the regulation of VSMC phenotypic switching, its functional role and underlying mechanism in AS-associated VSMC phenotypic switching remain incompletely understood. Methods An in vitro AS-related VSMC model was established by treating T/G HA-VSMCs with oxidized low-density lipoprotein (ox-LDL). Cell proliferation and migration were assessed using CCK-8, EdU incorporation, and Transwell assays. RNA and protein expression levels were determined by qRT-PCR and western blotting, respectively. The targeted relationship between miR-148b and KLF4 was examined using dual-luciferase reporter and RNA immunoprecipitation assays. KLF4 protein stability and ubiquitination were assessed using cycloheximide chase, MG132 treatment, and immunoprecipitation followed by western blotting. Results miR-148b expression was significantly reduced in ox-LDL-treated VSMCs. Overexpression of miR-148b suppressed ox-LDL-induced VSMC proliferation and migration, and restored the expression of contractile phenotype markers, including SM22α and α-SMA. Mechanistically, KLF4 was identified as a downstream target of miR-148b. miR-148b reduced KLF4 expression through 3′-UTR-mediated repression and was associated with enhanced ubiquitination-dependent KLF4 protein degradation. Rescue experiments showed that KLF4 overexpression partially reversed the inhibitory effects of miR-148b on VSMC proliferation, migration, and phenotypic switching. Conclusion miR-148b attenuates ox-LDL-induced VSMC phenotypic switching, at least in part, by downregulating KLF4. These findings suggest that the miR-148b/KLF4 axis may represent a potential regulatory mechanism in AS-associated vascular remodeling .
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PubMed
高影响因子
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
·
2022
·
IF 3.712
Fan Zhang,Jingxing Li,Chengxiong Gu,Haibo Zhang
Background The role and function of microRNA (miRNA, miR)-140-5p in the calcification of vascular smooth muscle cells (VSMCs) have been explored in this study.Methods The calcium nodules formed in transfected and β-glycerophosphate (β-GP)-treated VSMCs were observed using Alizarin Red S staining, and alkaline phosphatase (ALP) activity was determined. VSMC apoptosis was detected with flow cytometry assay. The target gene of miR-140-5p was predicted and confirmed with dual-luciferase reporter assay. Relative expressions of miR-140-5p, toll like receptor 4 (TLR4) and vascular calcification-related proteins (α-smooth muscle actin, α-SMA; Msh Homeobox 2, MSX2; bone morphogenetic protein 2, BMP2; Kruppel-like factor 4, KLF4; Runt-related transcription factor 2, RUNX2) were measured through quantitative real time polymerase chain reaction (qRT-PCR) and western blot.Results MiR-140-5p upregulation reversed the effects of β-GP on downregulating miR-140-5p and α-SMA expressions, enhancing ALP activity, calcium nodule formation and cell apoptosis, and upregulating levels of MSX2, BMP2, KLF4 and RUNX2. TLR4 was the target of miR-140-5p, and offset the effects of miR-140-5p on β-GP-induced VSMCs.Conclusions MiR-140-5p upregulation represses β-GP-induced calcification of VSMCs via targeting TLR4, providing a potential therapeutic method for vascular calcification.
研究领域:
分子生物学
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心血管疾病
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
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