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Your search keyword '"Li, Zhi-Ling"' showing total 401 results
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401 results on '"Li, Zhi-Ling"'

1. The pharmacogenomic landscape in the Chinese: An analytics of pharmacogenetic variants in 206,640 individuals

Author

Wang, Lei-Yun, Yu, Bing, Peng, Ying, Mou, Kai, Zhan, Yan, Wang, Yi-Min, Ji, Wei, Xu, Chun, Xiao, Le-Dong, Chen, Yan, Wang, Hua, She, Zhi-Hua, Dai, Peng, Zhao, Gan-Ye, Wang, Yang, Yu, Lu-Lu, Yu, Miao, Liu, Ke, Cui, Jia-Jia, Liu, Rong, Li, Xi, Huang, Yuan-Fei, Liu, Zhao-Qian, Ouyang, Dong-Sheng, Zhang, Wei, Li, Qing, Xiong, Xing-Liang, Guo, Cheng-Xian, Li, Jin-Gao, Lv, Qiao-Li, Xing, Qing-He, Wang, Hai-Jian, Li, Zhi-Ling, Wu, Ji-Chu, Huang, Long-Jian, He, Jian, Tan, Li-Ming, Hong, Wen-Xu, Wang, Xue-Chang, Li, Chao-Peng, Lu, Qin, Zhang, Long, Kong, Xiang-Dong, Zhou, Hong-Hao, and Yin, Ji-Ye

Published
2025
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20. Telitacicept for refractory cystitis associated with severe systemic lupus erythematosus: A case report.

Author

Ling, Gui-Chen, Zhang, Shan, Guo, Ying-Ao, Yang, Shuo, Li, Zhi-Ling, Zhang, Jian-Yong, and Xie, Jing-Jing

Subjects
SYSTEMIC lupus erythematosus, RETENTION of urine, CYSTITIS, ACQUISITION of data, CYCLOPHOSPHAMIDE
Abstract

Background: Lupus cystitis, a severe complication of systemic lupus erythematosus (SLE), presents considerable treatment challenges. Purpose: This case report describes the use of telitacicept in treating severe SLE with lupus cystitis. Research Design: A single patient with lupus cystitis. Study Sample: A patient with symptoms including frequent urination, urgency, and acute urinary retention. Data Collection and Analysis: Initial treatments included corticosteroid pulse therapy, immunoglobulin, and cyclophosphamide, which improved laboratory indicators but failed to alleviate symptoms of urinary retention. The patient was then treated with telitacicept. Results: Significant alleviation of urinary retention was observed shortly after incorporating telitacicept into the treatment regimen. The patient's condition remained stable with no relapse during the subsequent 10 months of follow-up. Conclusions: This case highlights the therapeutic potential of telitacicept for SLE patients who are unresponsive to conventional therapies, particularly those with severe manifestations such as lupus cystitis. [ABSTRACT FROM AUTHOR]

Published
2025
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46. TRPML1 triggers ferroptosis defense and is a potential therapeutic target in AKT-hyperactivated cancer.

Author

Zhang, Hai-Liang, Hu, Bing-Xin, Ye, Zhi-Peng, Li, Zhi-Ling, Liu, Shan, Zhong, Wen-Qing, Du, Tian, Yang, Dong, Mai, Jia, Li, Li-Chao, Chen, Yu-Hong, Zhu, Xian-Ying, Li, Xuan, Feng, Gong-Kan, Zhu, Xiao-Feng, and Deng, Rong

Subjects
PEPTIDES, FUNCTIONAL analysis, CANCER treatment, CELL death, CANCER cells, KINASE inhibitors
Abstract

Targeting ferroptosis for cancer therapy has slowed because of an incomplete understanding of ferroptosis mechanisms under specific pathological contexts such as tumorigenesis and cancer treatment. Here, we identify TRPML1-mediated lysosomal exocytosis as a potential anti-ferroptotic process through genome-wide CRISPR-Cas9 activation and kinase inhibitor library screening. AKT directly phosphorylated TRPML1 at Ser343 and inhibited K552 ubiquitination and proteasome degradation of TRPML1, thereby promoting TRPML1 binding to ARL8B to trigger lysosomal exocytosis. This boosted ferroptosis defense of AKT-hyperactivated cancer cells by reducing intracellular ferrous iron and enhancing membrane repair. Correlation analysis and functional analysis revealed that TRPML1-mediated ferroptosis resistance is a previously unrecognized feature of AKT-hyperactivated cancers and is necessary for AKT-driven tumorigenesis and cancer therapeutic resistance. TRPML1 inactivation or blockade of the interaction between TRPML1 and ARL8B inhibited AKT-driven tumorigenesis and cancer therapeutic resistance in vitro and in vivo by promoting ferroptosis. A synthetic peptide targeting TRPML1 inhibited AKT-driven tumorigenesis and enhanced the sensitivity of AKT-hyperactivated tumors to ferroptosis inducers, radiotherapy, and immunotherapy by boosting ferroptosis in vivo. Together, our findings identified TRPML1 as a therapeutic target in AKT-hyperactivated cancer. Editor's summary: Ferroptosis is a nonapoptotic form of regulated cell death and has been an attractive target for cancer therapy; however, the incomplete understanding of its underlying mechanism in tumorigenesis and resistance has limited its use. Here, Zhang et al. have identified transient receptor potential muclipin 1 (TRPML1) as a potential anti-ferroptotic process and target in AKT-driven cancer. They confirmed in vivo that TRPML1 inactivation using a synthetic peptide could increase sensitivity of AKT-hyperactivated tumors to ferroptosis inducers. This highlights TRPML1 as a promising therapeutic target that requires further evaluation. —Dorothy Hallberg [ABSTRACT FROM AUTHOR]

Published
2024
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49. TNFAIP3 Derived from Skeletal Stem Cells Alleviated Rat Osteoarthritis by Inhibiting the Necroptosis of Subchondral Osteoblasts

Author

Li, Xiao-Tong, primary, Li, Zhi-Ling, additional, Li, Pei-Lin, additional, Wang, Fei-Yan, additional, Zhang, Xiao-Yu, additional, Wang, Yu-Xing, additional, Zhao, Zhi-Dong, additional, Yin, Bo-Feng, additional, Hao, Rui-Cong, additional, Mao, Ning, additional, Xia, Wen-Rong, additional, Ding, Li, additional, and Zhu, Heng, additional

Published
2023
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