Journal of Zhejiang University. Science. B最新文献

{"title":"AAZ2 induces mitochondrial-dependent apoptosis by targeting PDK1 in gastric cancer.","authors":"Yi Li,&nbsp;Wenyan She,&nbsp;Xiaoran Xu,&nbsp;Yixin Liu,&nbsp;Xinyu Wang,&nbsp;Sheng Tian,&nbsp;Shiyi Li,&nbsp;Miao Wang,&nbsp;Chaochao Yu,&nbsp;Pan Liu,&nbsp;Tianhe Huang,&nbsp;Yongchang Wei","doi":"10.1631/jzus.B2200351","DOIUrl":"https://doi.org/10.1631/jzus.B2200351","url":null,"abstract":"<p><p>Drastic surges in intracellular reactive oxygen species (ROS) induce cell apoptosis, while most chemotherapy drugs lead to the accumulation of ROS. Here, we constructed an organic compound, arsenical <i>N</i>-‍(4-(1,3,2-dithiarsinan-2-yl)phenyl)acrylamide (AAZ2), which could prompt the ROS to trigger mitochondrial-dependent apoptosis in gastric cancer (GC). Mechanistically, by targeting pyruvate dehydrogenase kinase 1 (PDK1), AAZ2 caused metabolism alteration and the imbalance of redox homeostasis, followed by the inhibition of phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway and leading to the activation of B-cell lymphoma 2 (Bcl2)/Bcl2-associated X (Bax)/caspase-9 (Cas9)/Cas3 cascades. Importantly, our in vivo data demonstrated that AAZ2 could inhibit the growth of GC xenograft. Overall, our data suggested that AAZ2 could contribute to metabolic abnormalities, leading to mitochondrial-dependent apoptosis by targeting PDK1 in GC.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 3","pages":"232-247"},"PeriodicalIF":0.0,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014317/pdf/JZhejiangUnivSciB-24-3-232.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9116177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen upregulates DNA2 expression through the PI3K-AKT pathway in endometrial carcinoma.","authors":"Xinyan Wang,&nbsp;Xiuling Xu,&nbsp;Ting Zhang,&nbsp;Yang Jin,&nbsp;Sheng Xu,&nbsp;Lifeng Chen,&nbsp;Yucheng Lai,&nbsp;Ling Zhang,&nbsp;Ruolang Pan,&nbsp;Yan Yu","doi":"10.1631/jzus.B2200436","DOIUrl":"https://doi.org/10.1631/jzus.B2200436","url":null,"abstract":"<p><p>Endometrial cancer is the most common gynecological malignancy, affecting up to 3% of women at some point during their lifetime (Morice et al., 2016; Li and Wang, 2021). Based on the pathogenesis and biological behavioral characteristics, endometrial cancer can be divided into estrogen-dependent (I) and non-estrogen-dependent (II) types (Ulrich, 2011). Type I accounts for approximately 80% of cases, of which the majority are endometrioid carcinomas, and the remaining are mucinous adenocarcinomas (Setiawan et al., 2013). It is generally recognized that long-term stimulation by high estrogen levels with the lack of progesterone antagonism is the most important risk factor; meanwhile, there is no definite conclusion on the specific pathogenesis. The incidence of endometrial cancer has been on the rise during the past two decades (Constantine et al., 2019; Gao et al., 2022; Luo et al., 2022). Moreover, the development of assisted reproductive technology and antiprogestin therapy following breast cancer surgery has elevated the risk of developing type I endometrial cancer to a certain extent (Vassard et al., 2019). Therefore, investigating the influence of estrogen in type I endometrial cancer may provide novel concepts for risk assessment and adjuvant therapy, and at the same time, provide a basis for research on new drugs to treat endometrial cancer.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 3","pages":"262-268"},"PeriodicalIF":0.0,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014318/pdf/JZhejiangUnivSciB-24-3-262.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9116173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An epipolythiodioxopiperazine alkaloid and diversified aromatic polyketides with cytotoxicity from the Beibu Gulf coral-derived fungus <i>Emericella nidulans</i> GXIMD 02509.","authors":"Miaoping Lin,&nbsp;Zhenzhou Tang,&nbsp;Jiaxi Wang,&nbsp;Humu Lu,&nbsp;Chenwei Wang,&nbsp;Yanting Zhang,&nbsp;Xinming Liu,&nbsp;Chenghai Gao,&nbsp;Yonghong Liu,&nbsp;Xiaowei Luo","doi":"10.1631/jzus.B2200622","DOIUrl":"https://doi.org/10.1631/jzus.B2200622","url":null,"abstract":"北部湾藴育着丰富且亟待研究的海洋（微）生物资源,是活性天然产物的重要来源。本研究从涠洲岛珊瑚共附生构巢裸胞壳菌GXIMD 02509中分离获得一个多硫代二酮哌嗪生物碱和系列芳香聚酮类化合物,包含一个新化合物4a- O -methoxyarugosin H ( 1 )。我们通过采用多种波、光谱学技术及对比文献方法鉴定了化合物的化学结构。化合物 1 ∼ 5 、7和 10 对786-O、SW1990和SW480等3株肿瘤细胞增殖具抑制活性,半抑制浓度（IC_50）值为4.3∼33.4 µmol/L。化合物emestrin J ( 10 )具有一个二硫桥键,还能够显著抑制786-O细胞克隆及迁移,诱导786-O细胞凋亡并阻滞细胞分裂在G2/M期,是一个潜在具抗肿瘤活性的先导化合物。","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 3","pages":"275-280"},"PeriodicalIF":0.0,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014321/pdf/JZhejiangUnivSciB-24-3-275.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9121018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerobic glycolysis in colon cancer is repressed by naringin via the <i>HIF1Α</i> pathway.","authors":"Guangtao Pan,&nbsp;Ping Zhang,&nbsp;Aiying Chen,&nbsp;Yu Deng,&nbsp;Zhen Zhang,&nbsp;Han Lu,&nbsp;Aoxun Zhu,&nbsp;Cong Zhou,&nbsp;Yanran Wu,&nbsp;Sen Li","doi":"10.1631/jzus.B2200221","DOIUrl":"https://doi.org/10.1631/jzus.B2200221","url":null,"abstract":"<p><p>Metabolic reprogramming is a common phenomenon in cancer, with aerobic glycolysis being one of its important characteristics. Hypoxia-inducible factor-1α (<i>HIF1Α</i>) is thought to play an important role in aerobic glycolysis. Meanwhile, naringin is a natural flavanone glycoside derived from grapefruits and many other citrus fruits. In this work, we identified glycolytic genes related to <i>HIF1Α</i> by analyzing the colon cancer database. The analysis of extracellular acidification rate and cell function verified the regulatory effects of <i>HIF1Α</i> overexpression on glycolysis, and the proliferation and migration of colon cancer cells. Moreover, naringin was used as an inhibitor of colon cancer cells to illustrate its effect on <i>HIF1Α</i> function. The results showed that the <i>HIF1Α</i> and enolase 2 (<i>ENO2</i>) levels in colon cancer tissues were highly correlated, and their high expression indicated a poor prognosis for colon cancer patients. Mechanistically, <i>HIF1Α</i> directly binds to the DNA promoter region and upregulates the transcription of <i>ENO2</i>; ectopic expression of <i>ENO2</i> increased aerobic glycolysis in colon cancer cells. Most importantly, we found that the appropriate concentration of naringin inhibited the transcriptional activity of <i>HIF1Α</i>, which in turn decreased aerobic glycolysis in colon cancer cells. Generally, naringin reduces glycolysis in colon cancer cells by reducing the transcriptional activity of <i>HIF1Α</i> and the proliferation and invasion of colon cancer cells. This study helps to elucidate the relationship between colon cancer progression and glucose metabolism, and demonstrates the efficacy of naringin in the treatment of colon cancer.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 3","pages":"221-231"},"PeriodicalIF":0.0,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014316/pdf/JZhejiangUnivSciB-24-3-221.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9119361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfiram enhances the antitumor activity of cisplatin by inhibiting the Fanconi anemia repair pathway.","authors":"Meng Yuan,&nbsp;Qian Wu,&nbsp;Mingyang Zhang,&nbsp;Minshan Lai,&nbsp;Wenbo Chen,&nbsp;Jianfeng Yang,&nbsp;Li Jiang,&nbsp;Ji Cao","doi":"10.1631/jzus.B2200405","DOIUrl":"https://doi.org/10.1631/jzus.B2200405","url":null,"abstract":"<p><p>A series of chemotherapeutic drugs that induce DNA damage, such as cisplatin (DDP), are standard clinical treatments for ovarian cancer, testicular cancer, and other diseases that lack effective targeted drug therapy. Drug resistance is one of the main factors limiting their application. Sensitizers can overcome the drug resistance of tumor cells, thereby enhancing the antitumor activity of chemotherapeutic drugs. In this study, we aimed to identify marketable drugs that could be potential chemotherapy sensitizers and explore the underlying mechanisms. We found that the alcohol withdrawal drug disulfiram (DSF) could significantly enhance the antitumor activity of DDP. JC-1 staining, propidium iodide (PI) staining, and western blotting confirmed that the combination of DSF and DDP could enhance the apoptosis of tumor cells. Subsequent RNA sequencing combined with Gene Set Enrichment Analysis (GSEA) pathway enrichment analysis and cell biology studies such as immunofluorescence suggested an underlying mechanism: DSF makes cells more vulnerable to DNA damage by inhibiting the Fanconi anemia (FA) repair pathway, exerting a sensitizing effect to DNA damaging agents including platinum chemotherapy drugs. Thus, our study illustrated the potential mechanism of action of DSF in enhancing the antitumor effect of DDP. This might provide an effective and safe solution for combating DDP resistance in clinical treatment.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 3","pages":"207-220"},"PeriodicalIF":0.0,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014319/pdf/JZhejiangUnivSciB-24-3-207.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9116180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chinese consensus guidelines for therapeutic drug monitoring of polymyxin B, endorsed by the Infection and Chemotherapy Committee of the Shanghai Medical Association and the Therapeutic Drug Monitoring Committee of the Chinese Pharmacological Society.","authors":"Xiaofen Liu,&nbsp;Chenrong Huang,&nbsp;Phillip J Bergen,&nbsp;Jian Li,&nbsp;Jingjing Zhang,&nbsp;Yijian Chen,&nbsp;Yongchuan Chen,&nbsp;Beining Guo,&nbsp;Fupin Hu,&nbsp;Jinfang Hu,&nbsp;Linlin Hu,&nbsp;Xin Li,&nbsp;Hongqiang Qiu,&nbsp;Hua Shao,&nbsp;Tongwen Sun,&nbsp;Yu Wang,&nbsp;Ping Xu,&nbsp;Jing Yang,&nbsp;Yong Yang,&nbsp;Zhenwei Yu,&nbsp;Bikui Zhang,&nbsp;Huaijun Zhu,&nbsp;Xiaocong Zuo,&nbsp;Yi Zhang,&nbsp;Liyan Miao,&nbsp;Jing Zhang","doi":"10.1631/jzus.B2200466","DOIUrl":"https://doi.org/10.1631/jzus.B2200466","url":null,"abstract":"<p><p>Polymyxin B, which is a last-line antibiotic for extensively drug-resistant Gram-negative bacterial infections, became available in China in Dec. 2017. As dose adjustments are based solely on clinical experience of risk toxicity, treatment failure, and emergence of resistance, there is an urgent clinical need to perform therapeutic drug monitoring (TDM) to optimize the use of polymyxin B. It is thus necessary to standardize operating procedures to ensure the accuracy of TDM and provide evidence for their rational use. We report a consensus on TDM guidelines for polymyxin B, as endorsed by the Infection and Chemotherapy Committee of the Shanghai Medical Association and the Therapeutic Drug Monitoring Committee of the Chinese Pharmacological Society. The consensus panel was composed of clinicians, pharmacists, and microbiologists from different provinces in China and Australia who made recommendations regarding target concentrations, sample collection, reporting, and explanation of TDM results. The guidelines provide the first-ever consensus on conducting TDM of polymyxin B, and are intended to guide optimal clinical use.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 2","pages":"130-142"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260281/pdf/JZhejiangUnivSciB-24-2-130.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9677379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple characteristic alterations and available therapeutic strategies of cellular senescence.","authors":"Yunzi Zhao,&nbsp;Hui Li,&nbsp;Qinglong Guo,&nbsp;Hui Hui","doi":"10.1631/jzus.B2200178","DOIUrl":"https://doi.org/10.1631/jzus.B2200178","url":null,"abstract":"<p><p>Given its state of stable proliferative inhibition, cellular senescence is primarily depicted as a critical mechanism by which organisms delay the progression of carcinogenesis. Cells undergoing senescence are often associated with the alteration of a series of specific features and functions, such as metabolic shifts, stemness induction, and microenvironment remodeling. However, recent research has revealed more complexity associated with senescence, including adverse effects on both physiological and pathological processes. How organisms evade these harmful consequences and survive has become an urgent research issue. Several therapeutic strategies targeting senescence, including senolytics, senomorphics, immunotherapy, and function restoration, have achieved initial success in certain scenarios. In this review, we describe in detail the characteristic changes associated with cellular senescence and summarize currently available countermeasures.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 2","pages":"101-114"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9936135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9615425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liensinine attenuates inflammation and oxidative stress in spleen tissue in an LPS-induced mouse sepsis model.","authors":"Hanyu Wang,&nbsp;Yuanhao Yang,&nbsp;Xiao Zhang,&nbsp;Yan Wang,&nbsp;Hui Fan,&nbsp;Jinfeng Shi,&nbsp;Xuelian Tan,&nbsp;Baoshi Xu,&nbsp;Jingchao Qiang,&nbsp;Enzhuang Pan,&nbsp;Mingyi Chu,&nbsp;Zibo Dong,&nbsp;Jingquan Dong","doi":"10.1631/jzus.B2200340","DOIUrl":"https://doi.org/10.1631/jzus.B2200340","url":null,"abstract":"<p><p>Sepsis is a complex syndrome caused by multiple pathogens and involves multiple organ failure, particularly spleen dysfunction. In 2017, the worldwide incidence was 48.9 million sepsis cases and 11 million sepsis-related deaths were reported (Rudd et al., 2020). Inflammation, oxidative stress, and apoptosis are the most common pathologies seen in sepsis. Liensinine (LIE) is a bisbenzylisoquinoline-type alkaloid extracted from the seed embryo of Nelumbo nucifera. Lotus seed hearts have high content of LIE which mainly has antihypertensive and antiarrhythmic pharmacological effects. It can exert anti-carcinogenic activity by regulating cell, inflammation, and apoptosis signaling pathways (Manogaran et al., 2019). However, its protective effect from sepsis-induced spleen damage is unknown. In this research, we established a mouse sepsis model induced by lipopolysaccharide (LPS) and investigated the protective effects of LIE on sepsis spleen injury in terms of inflammatory response, oxidative stress, and apoptosis.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 2","pages":"185-190"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260283/pdf/JZhejiangUnivSciB-24-2-185.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9979139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>AIFM1</i> variants associated with auditory neuropathy spectrum disorder cause apoptosis due to impaired apoptosis-inducing factor dimerization.","authors":"Yue Qiu,&nbsp;Hongyang Wang,&nbsp;Huaye Pan,&nbsp;Jing Guan,&nbsp;Lei Yan,&nbsp;Mingjie Fan,&nbsp;Hui Zhou,&nbsp;Xuanhao Zhou,&nbsp;Kaiwen Wu,&nbsp;Zexiao Jia,&nbsp;Qianqian Zhuang,&nbsp;Zhaoying Lei,&nbsp;Mengyao Li,&nbsp;Xue Ding,&nbsp;Aifu Lin,&nbsp;Yong Fu,&nbsp;Dong Zhang,&nbsp;Qiuju Wang,&nbsp;Qingfeng Yan","doi":"10.1631/jzus.B2200081","DOIUrl":"https://doi.org/10.1631/jzus.B2200081","url":null,"abstract":"<p><p>Auditory neuropathy spectrum disorder (ANSD) represents a variety of sensorineural deafness conditions characterized by abnormal inner hair cells and/or auditory nerve function, but with the preservation of outer hair cell function. ANSD represents up to 15% of individuals with hearing impairments. Through mutation screening, bioinformatic analysis and expression studies, we have previously identified several apoptosis-inducing factor (AIF) mitochondria-associated 1 (<i>AIFM1</i>) variants in ANSD families and in some other sporadic cases. Here, to elucidate the pathogenic mechanisms underlying each <i>AIFM1</i> variant, we generated AIF-null cells using the clustered regularly interspersed short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) system and constructed AIF-wild type (WT) and AIF-mutant (mut) (p.‍T260A, p.‍R422W, and p.‍R451Q) stable transfection cell lines. We then analyzed AIF structure, coenzyme-binding affinity, apoptosis, and other aspects. Results revealed that these variants resulted in impaired dimerization, compromising AIF function. The reduction reaction of AIF variants had proceeded slower than that of AIF-WT. The average levels of AIF dimerization in AIF variant cells were only 34.5%‍‒‍49.7% of that of AIF-WT cells, resulting in caspase-independent apoptosis. The average percentage of apoptotic cells in the variants was 12.3%‍‒‍17.9%, which was significantly higher than that (6.9%‍‒‍7.4%) in controls. However, nicotinamide adenine dinucleotide (NADH) treatment promoted the reduction of apoptosis by rescuing AIF dimerization in AIF variant cells. Our findings show that the impairment of AIF dimerization by <i>AIFM1</i> variants causes apoptosis contributing to ANSD, and introduce NADH as a potential drug for ANSD treatment. Our results help elucidate the mechanisms of ANSD and may lead to the provision of novel therapies.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 2","pages":"172-184"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260280/pdf/JZhejiangUnivSciB-24-2-172.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9677376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel perspective in transplantation therapy of mesenchymal stem cells: targeting the ferroptosis pathway.","authors":"Yuzhu Xu,&nbsp;Pan Fan,&nbsp;Lei Liu,&nbsp;X U Xuanfei,&nbsp;Lele Zhang,&nbsp;Jiadong Wang,&nbsp;Yuao Tao,&nbsp;Xiaolong Li,&nbsp;Xi Li,&nbsp;Yuntao Wang","doi":"10.1631/jzus.B2200410","DOIUrl":"https://doi.org/10.1631/jzus.B2200410","url":null,"abstract":"<p><p>Ex vivo culture-amplified mesenchymal stem cells (MSCs) have been studied because of their capacity for healing tissue injury. MSC transplantation is a valid approach for promoting the repair of damaged tissues and replacement of lost cells or to safeguard surviving cells, but currently the efficiency of MSC transplantation is constrained by the extensive loss of MSCs during the short post-transplantation period. Hence, strategies to increase the efficacy of MSC treatment are urgently needed. Iron overload, reactive oxygen species deposition, and decreased antioxidant capacity suppress the proliferation and regeneration of MSCs, thereby hastening cell death. Notably, oxidative stress (OS) and deficient antioxidant defense induced by iron overload can result in ferroptosis. Ferroptosis may inhibit cell survival after MSC transplantation, thereby reducing clinical efficacy. In this review, we explore the role of ferroptosis in MSC performance. Given that little research has focused on ferroptosis in transplanted MSCs, further study is urgently needed to enhance the in vivo implantation, function, and duration of MSCs.</p>","PeriodicalId":17601,"journal":{"name":"Journal of Zhejiang University. Science. B","volume":"24 2","pages":"115-129"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10260286/pdf/JZhejiangUnivSciB-24-2-115.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9677378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}