Shi Mengkun相关文献与解析，生知库 | 链接生命科学的每一步

miR-3606-3p alleviates skin fibrosis by integratively suppressing the integrin/FAK, p-AKT/p-ERK, and TGF-Î² signaling cascades.

miR-3606-3p 通过整合抑制整合素/FAK、p-AKT/p-ERK 和 TGF-β 信号级联来缓解皮肤纤维化。

doi:10.1016/j.jare.2024.11.027

Chen Yahui, Gong Yiyi, Shi Mengkun, Zhu Haoxing, Tang Yulong, Huang Delin, Wang Wei, Shi Chenyi, Xia Xueyi, Zhang Ying, Liu Jianlan, Huang Jia, Liu Mengguo, Chen Huyan, Ma Yanyun, Wang Ziyu, Wang Lei, Tu Wenzhen, Zhao Yinhuan, Lin Jinran, Jin Li, Distler JÃ¶rg Hw, Wu Wenyu, Wang Jiucun, Shi Xiangguang

Ferroptosis-Resistant Adipocytes Drive Keloid Pathogenesis via GPX4-Mediated Adipocyte-Mesenchymal Transition and Iron-Cystine Metabolic Communication.

抗铁死亡脂肪细胞通过 GPX4 介导的脂肪细胞-间质转化和铁-胱氨酸代谢通讯驱动瘢痕疙瘩的发病机制

期刊:International Journal of Biological Sciences

影响因子:10

doi:10.7150/ijbs.114930

Shi Xiangguang, Xia Xueyi, Xiao Yang, Shu Huizhen, Xu Zhuoya, Liu Mengguo, Shi Chenyi, Zhang Ying, Wei Yining, Gong Yiyi, Wang Wei, Chen Yahui, Liu Jianlan, Huang Jia, Shi Mengkun, Wang Jiucun, Wu Wenyu

Increased melanin induces aberrant keratinocyteâ-âmelanocyteâ-âbasalâ-âfibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids.

黑色素增多会诱导瘢痕疙瘩中角质形成细胞-黑色素细胞-基底细胞-成纤维细胞之间的异常通讯和纤维化，其机制是通过诱导铁过载和铁死亡抵抗

期刊:Cell Communication and Signaling

影响因子:8.9

doi:10.1186/s12964-025-02116-z

Shi Xiangguang, Xia Xueyi, Xiao Yang, Zhang Ying, Gong Yiyi, Chen Yahui, Shi Chenyi, Wang Wei, Liu Jianlan, Huang Jia, Liu Mengguo, Xu Zhuoya, Ma Yanyun, Shi Mengkun, Wang Jiucun, Wu Wenyu

The TEAD4-DYNLL1 axis accelerates cell cycle progression and augments malignant properties of lung adenocarcinoma cells.

TEAD4-DYNLL1轴加速细胞周期进程，增强肺腺癌细胞的恶性特性

期刊:European Journal of Medical Research

影响因子:3.4

doi:10.1186/s40001-025-02500-y

Li Dapeng, Wang An, Wang Xuan, Shi Mengkun, Chen Xiaofeng, Lyu Yubao, Huang Dayu

The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases

肺纤维化的新型分子机制：通过对单细胞RNA测序数据库的重新分析深入了解脂质代谢

期刊:Lipids in Health and Disease

影响因子:4.2

doi:10.1186/s12944-024-02062-8

Shi, Xiangguang; Chen, Yahui; Shi, Mengkun; Gao, Fei; Huang, Lihao; Wang, Wei; Wei, Dong; Shi, Chenyi; Yu, Yuexin; Xia, Xueyi; Song, Nana; Chen, Xiaofeng; Distler, Jörg H W; Lu, Chenqi; Chen, Jingyu; Wang, Jiucun

Prediction of Overall Survival of Patients with Completely Resected Non-Small Cell Lung Cancer: Analyses of Preoperative Spirometry, Preoperative Blood Tests, and Other Clinicopathological Data

预测完全切除的非小细胞肺癌患者的总生存期：术前肺功能检查、术前血液检查和其他临床病理数据的分析

期刊:Cancer Management and Research

影响因子:2.6

doi:10.2147/CMAR.S232219

Shi, Mengkun; Zhan, Cheng; Shi, Jialun; Wang, Qun

Bioinformatics analyses of the differences between lung adenocarcinoma and squamous cell carcinoma using The Cancer Genome Atlas expression data

利用癌症基因组图谱表达数据对肺腺癌和鳞状细胞癌之间的差异进行生物信息学分析

期刊:Molecular Medicine Reports

影响因子:3.5

doi:10.3892/mmr.2017.6629

Sun, Fenghao; Yang, Xiaodong; Jin, Yulin; Chen, Li; Wang, Lin; Shi, Mengkun; Zhan, Cheng; Shi, Yu; Wang, Qun

Interpreting circulating microbiome-related metabolites in coronary heart disease

解读冠心病中循环微生物组相关代谢物

miR-3606-3p alleviates skin fibrosis by integratively suppressing the integrin/FAK, p-AKT/p-ERK, and TGF-Î² signaling cascades.

miR-3606-3p 通过整合抑制整合素/FAK、p-AKT/p-ERK 和 TGF-β 信号级联来缓解皮肤纤维化。

Ferroptosis-Resistant Adipocytes Drive Keloid Pathogenesis via GPX4-Mediated Adipocyte-Mesenchymal Transition and Iron-Cystine Metabolic Communication.

抗铁死亡脂肪细胞通过 GPX4 介导的脂肪细胞-间质转化和铁-胱氨酸代谢通讯驱动瘢痕疙瘩的发病机制

Increased melanin induces aberrant keratinocyteâ-âmelanocyteâ-âbasalâ-âfibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids.

黑色素增多会诱导瘢痕疙瘩中角质形成细胞-黑色素细胞-基底细胞-成纤维细胞之间的异常通讯和纤维化，其机制是通过诱导铁过载和铁死亡抵抗

The TEAD4-DYNLL1 axis accelerates cell cycle progression and augments malignant properties of lung adenocarcinoma cells.

TEAD4-DYNLL1轴加速细胞周期进程，增强肺腺癌细胞的恶性特性

The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases

肺纤维化的新型分子机制：通过对单细胞RNA测序数据库的重新分析深入了解脂质代谢

Prediction of Overall Survival of Patients with Completely Resected Non-Small Cell Lung Cancer: Analyses of Preoperative Spirometry, Preoperative Blood Tests, and Other Clinicopathological Data

预测完全切除的非小细胞肺癌患者的总生存期：术前肺功能检查、术前血液检查和其他临床病理数据的分析

Bioinformatics analyses of the differences between lung adenocarcinoma and squamous cell carcinoma using The Cancer Genome Atlas expression data

利用癌症基因组图谱表达数据对肺腺癌和鳞状细胞癌之间的差异进行生物信息学分析

Interpreting circulating microbiome-related metabolites in coronary heart disease

解读冠心病中循环微生物组相关代谢物

miR-3606-3p alleviates skin fibrosis by integratively suppressing the integrin/FAK, p-AKT/p-ERK, and TGF-Î² signaling cascades.

miR-3606-3p 通过整合抑制整合素/FAK、p-AKT/p-ERK 和 TGF-β 信号级联来缓解皮肤纤维化。

Ferroptosis-Resistant Adipocytes Drive Keloid Pathogenesis via GPX4-Mediated Adipocyte-Mesenchymal Transition and Iron-Cystine Metabolic Communication.

抗铁死亡脂肪细胞通过 GPX4 介导的脂肪细胞-间质转化和铁-胱氨酸代谢通讯驱动瘢痕疙瘩的发病机制

Increased melanin induces aberrant keratinocyteâ-âmelanocyteâ-âbasalâ-âfibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids.

黑色素增多会诱导瘢痕疙瘩中角质形成细胞-黑色素细胞-基底细胞-成纤维细胞之间的异常通讯和纤维化，其机制是通过诱导铁过载和铁死亡抵抗

The TEAD4-DYNLL1 axis accelerates cell cycle progression and augments malignant properties of lung adenocarcinoma cells.

TEAD4-DYNLL1轴加速细胞周期进程，增强肺腺癌细胞的恶性特性

The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases

肺纤维化的新型分子机制：通过对单细胞RNA测序数据库的重新分析深入了解脂质代谢

Prediction of Overall Survival of Patients with Completely Resected Non-Small Cell Lung Cancer: Analyses of Preoperative Spirometry, Preoperative Blood Tests, and Other Clinicopathological Data

预测完全切除的非小细胞肺癌患者的总生存期：术前肺功能检查、术前血液检查和其他临床病理数据的分析

Bioinformatics analyses of the differences between lung adenocarcinoma and squamous cell carcinoma using The Cancer Genome Atlas expression data

利用癌症基因组图谱表达数据对肺腺癌和鳞状细胞癌之间的差异进行生物信息学分析

Increased melanin induces aberrant keratinocyteâ-âmelanocyteâ-âbasalâ-âfibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids.