Biochemical pharmacology最新文献

Cuproptosis involvement in neonatal ischemic-hypoxic encephalopathy through the COMMD1/ATP7A signaling axis comd1 /ATP7A信号轴参与新生儿缺血-缺氧性脑病

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-20 DOI: 10.1016/j.bcp.2025.117054

Jingjing Luo , Xiaoling Zhang , Laxman Bharati , Ziyu Hua , Sha Chen , Zhi Dong

{"title":"Cuproptosis involvement in neonatal ischemic-hypoxic encephalopathy through the COMMD1/ATP7A signaling axis","authors":"Jingjing Luo , Xiaoling Zhang , Laxman Bharati , Ziyu Hua , Sha Chen , Zhi Dong","doi":"10.1016/j.bcp.2025.117054","DOIUrl":"10.1016/j.bcp.2025.117054","url":null,"abstract":"<div><div>Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe brain lesion caused by perinatal asphyxia that often results in neonatal death or long-term neurological deficits. The in-depth study of cell death mechanisms has recently led to the discovery of cuproptosis, a new type of cell death. Although understanding the relationship between HIE and cuproptosis is still in its preliminary stages, there is evidence that copper ions and their associated metabolic pathways play an important role in the pathophysiology of HIE. We used the Rice-Vannucci method to construct a mouse model of HIE. Cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining and pathological changes in brain tissue were examined by hematoxylin and eosin and Nissl staining. The levels of cuproptosis indicators and of key proteins, Copper Metabolism MURR1 domain protein 1 (COMMD1) and ATPase Copper Transporting Alpha (ATP7A), in the signaling axis related to cuproptosis were determined by western blotting. Mitochondrial morphology was observed by transmission electron microscopy, and copper salt staining and a copper ion probe were used to detect copper ion levels. Methyl thiazolyl tetrazolium (MTT) assays were used to measure neuronal survival. Our results indicate that cuproptosis occurs during neonatal ischemia and hypoxia, and that cuproptosis can regulate the occurrence and development of neonatal ischemic-hypoxic encephalopathy through the COMMD1/ATP7A signaling axis. This study provides new understanding of neonatal ischemic-hypoxic encephalopathy and indicates targets for the development of therapeutics.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"239 ","pages":"Article 117054"},"PeriodicalIF":5.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FATS alleviates ulcerative colitis by inhibiting M1 macrophage polarization and aerobic glycolysis through promoting the ubiquitination-mediated degradation of HIF-1α. 脂肪通过促进泛素化介导的HIF-1α降解，抑制M1巨噬细胞极化和有氧糖酵解，从而缓解溃疡性结肠炎。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-19 DOI: 10.1016/j.bcp.2025.117053

Yingdi Han, Jing Xun, Tian Li, Xiaolin Jiang, Bin Liu, Zhibo Hu, Huichao Yang, Qi Gao, Zhao Wu, Xueliang Wu, Aimin Zhang, Ximo Wang, Zhiyu Guan, Xiangyang Yu, Qi Zhang

{"title":"FATS alleviates ulcerative colitis by inhibiting M1 macrophage polarization and aerobic glycolysis through promoting the ubiquitination-mediated degradation of HIF-1α.","authors":"Yingdi Han, Jing Xun, Tian Li, Xiaolin Jiang, Bin Liu, Zhibo Hu, Huichao Yang, Qi Gao, Zhao Wu, Xueliang Wu, Aimin Zhang, Ximo Wang, Zhiyu Guan, Xiangyang Yu, Qi Zhang","doi":"10.1016/j.bcp.2025.117053","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.117053","url":null,"abstract":"<p><p>Ulcerative colitis (UC) represents a challenging disorder characterized by a multifaceted pathogenesis. Macrophages, the predominant immune cell population in the intestinal milieu of individuals with UC, play a pivotal role in sustaining intestinal homeostasis. Common fragile sites (CFSs) are evolutionarily preserved genomic segments that exhibit a propensity for breakage and are present in all human beings. FATS (fragile site-associated tumor suppressor) is a novel CFS that functions as a tumor suppressor gene and an E3 ubiquitin ligase. But there are no studies on the regulation of inflammatory diseases by this gene. In this study, we used Fats whole-body knockout mice to construct DSS-induced UC model and elucidate the role of Fats in the progression of UC through immune regulation. We found that UC was more severe in Fats<sup>-/-</sup> mice than in WT control mice. The aggravation of UC observed in Fats<sup>-/-</sup> mice is contingent upon macrophage activity and corresponds with a phenotypic transition in colonic macrophages from an anti-inflammatory M2-like state to a pro-inflammatory M1-like state. In addition, co-IP (co-immunoprecipitation), PLA (Proximity ligation assay) and ubiquitylation experiments confirmed that Fats deficiency stabilizes the HIF-1α protein by reducing its degree of ubiquitination, which in turn heightens the expression of the transporters Glut1 and the enzymes Hk2 (hexokinase 2) and Ldha (lactate dehydrogenase) during glycolysis, thereby fostering macrophage polarization towards the M1 phenotype and exacerbating UC. Notably, inhibition of HIF-1α expression reversed the exacerbation of UC in Fats<sup>-/-</sup> mice. Collectively, these findings indicate that Fats plays a crucial role in modulating immune responses, positioning it as a potential therapeutic target in UC management.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"117053"},"PeriodicalIF":5.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ubiquitin ligase TRIM63 regulates HOXA10 expression to mediate fatty acid β-oxidation and suppress lung adenocarcinoma metastasis 泛素连接酶TRIM63调控HOXA10表达，介导脂肪酸β-氧化，抑制肺腺癌转移。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-18 DOI: 10.1016/j.bcp.2025.117052

Weijian Tang, Zhao Chen, Shaohua Xu, Zhoumiao Chen

{"title":"Ubiquitin ligase TRIM63 regulates HOXA10 expression to mediate fatty acid β-oxidation and suppress lung adenocarcinoma metastasis","authors":"Weijian Tang, Zhao Chen, Shaohua Xu, Zhoumiao Chen","doi":"10.1016/j.bcp.2025.117052","DOIUrl":"10.1016/j.bcp.2025.117052","url":null,"abstract":"<div><div>While it is clear that HOXA10 plays a role in the growth and metastasis of lung adenocarcinoma (LUAD), the details of its regulation are still largely a mystery. Our research sheds new light on this issue by revealing increased HOXA10 protein levels within LUAD tumors. Assays involving colony formation, wound healing, Transwell migration, and western blot (WB) demonstrated that LUAD cell proliferation, migration, and invasion were inhibited by HOXA10 knockdown, as were the expressions of proteins associated with epithelial-mesenchymal transition and metastasis. Overexpression of HOXA10 had the opposite impact. Nude mouse models of subcutaneous allografts and pulmonary metastasis showed that LUAD growth and metastasis were strongly curtailed by HOXA10 knockdown. Gene set enrichment analysis also highlighted a relationship between HOXA10 and the fatty acid β-oxidation (FAO) pathway. Analyses using BODIPY 493/503 staining and WB techniques demonstrated that knocking down HOXA10 in LUAD cells increased lipid accumulation and reduced FAO and key gene expression. The suppressive effects of HOXA10 knockdown on LUAD cell migration were neutralized by the addition of recombinant human Carnitine Palmitoyltransferase 1B (CPT1B) (rhCPT1B) protein. Our research also revealed an interaction between HOXA10 and tripartite motif containing 63 (TRIM63), where TRIM63 overexpression led to HOXA10 degradation through ubiquitination. Overexpression of TRIM63 decreased LUAD cell migration, but this effect was counteracted by HOXA10 overexpression. In summary, the discovery that TRIM63 orchestrates HOXA10 degradation to regulate FAO and curb LUAD matastasis suggests that interventions along the TRIM63-HOXA10 axis could be a fruitful approach to LUAD therapy.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"239 ","pages":"Article 117052"},"PeriodicalIF":5.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dimethylmalonate induces ferroptosis by inhibiting the SUCNR1/PI3K/HIF-1α/SLC7A11 signaling axis in triple-negative breast cancer 二甲基丙二酸盐通过抑制三阴性乳腺癌中SUCNR1/PI3K/HIF-1α/SLC7A11信号轴诱导铁下垂

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-16 DOI: 10.1016/j.bcp.2025.117051

Weiqiang Huang , Qizhuan Lin , Yu Cao , Changyong Gong , Libo Jin , Yongpan Wang , Renyi Peng

{"title":"Dimethylmalonate induces ferroptosis by inhibiting the SUCNR1/PI3K/HIF-1α/SLC7A11 signaling axis in triple-negative breast cancer","authors":"Weiqiang Huang , Qizhuan Lin , Yu Cao , Changyong Gong , Libo Jin , Yongpan Wang , Renyi Peng","doi":"10.1016/j.bcp.2025.117051","DOIUrl":"10.1016/j.bcp.2025.117051","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by the absence of the estrogen receptor (ER), progesterone receptor (PR), and HER2 protein, resulting in limited treatment options and a poor prognosis. In recent years, ferroptosis, a newly discovered form of programmed cell death, along with its key regulatory molecules, has emerged as a promising target for cancer treatment. Dimethyl malonate (DMM) is commonly used in studies of neurological disorders and oxidative stress-related diseases, but its application in the treatment of breast cancer, including TNBC, has not been explored. This study revealed that DMM significantly inhibits the proliferation and migration of TNBC cells. The underlying mechanism may involve disruption of the antioxidant defense system in TNBC cells, thereby promoting lipid peroxidation-induced ferroptosis. Furthermore, a zebrafish embryo coculture model confirmed the inhibitory effect of DMM on TNBC cell proliferation and migration in vivo, demonstrating its antitumor potential. At the molecular level, Western blotting, immunofluorescence, and qPCR confirmed that DMM inhibits the downstream PI3K/HIF-1α pathway mediated by the succinate receptor SUCNR1, thereby inhibiting the expression of the antioxidant molecules SLC7A11 and GPX4. This leads to the induction of ferroptosis, which suppresses TNBC cell proliferation and migration. Finally, overexpression experiments further validated the core regulatory role of SUCNR1 in this process.</div><div>This study reveals the molecular mechanism by which DMM induces ferroptosis in TNBC cells through the SUCNR1/PI3K/HIF-1α signaling pathway, providing new theoretical insights for the exploration of TNBC pathogenesis and clinical treatment strategies.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"239 ","pages":"Article 117051"},"PeriodicalIF":5.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polypharmacology translates between species and phylogenetic distance: A functional, bioinformatic, and structural study on organic anion transporting polypeptides. 多药理学在物种和系统发育距离之间的转化：有机阴离子转运多肽的功能、生物信息学和结构研究。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-12 DOI: 10.1016/j.bcp.2025.117049

Katja Stefan, Vigneshwaran Namasivayam, Mst Tazmin Akhter, Gergely Gyimesi, Muhammad Rafehi, Hauke Busch, Tomasz Trombik, Till Luckenbach, Jörg König, Sven Marcel Stefan

{"title":"Polypharmacology translates between species and phylogenetic distance: A functional, bioinformatic, and structural study on organic anion transporting polypeptides.","authors":"Katja Stefan, Vigneshwaran Namasivayam, Mst Tazmin Akhter, Gergely Gyimesi, Muhammad Rafehi, Hauke Busch, Tomasz Trombik, Till Luckenbach, Jörg König, Sven Marcel Stefan","doi":"10.1016/j.bcp.2025.117049","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.117049","url":null,"abstract":"<p><p>Recently, we postulated the existence of 'multitarget binding sites', reoccurring structural motifs that interconnect otherwise structurally, functionally, and/or phylogenetically distant proteins. In this study, we functionally assessed a selection of 23 multitarget ATP-binding cassette (pan-ABC) transporter modulators against zebrafish (Danio rerio) organic anion transporting polypeptide (drOatp1d1), a transport protein of the solute carrier (SLC) superfamily. Zebrafishes are important in vivo models in drug development to evaluate drug pharmacokinetics and pharmacodynamics. In total, 87.0% of the compounds were identified as drOatp1d1 transport inhibitors despite the relative phylogenetic distance of drOatp1d1 to other Oatps/OATPs. The observed effects resembled the ones observed for human OATP1A2, OATP1B1, OATP1B3, and OATP2B1, and potent hit molecules appeared to bind to a potential drOatp1d1 binding site derived from a OATP1B1 cryo-EM structure - strengthening the notion of common structural motifs between membrane transporters. The bioactivity of Pranlukast (PRA) on human OATPs could be accurately predicted based on its activity on drOatp1d1. The collection of pan-ABC transporter modulators also showed activity against other zebrafish (i.e., drAbcb4) and non-zebrafish (i.e., mumAbca1) membrane transporters, ultimately rendering it a suitable tool to translate between species to tackle the undruggability of membrane transporters and potentially other proteins by addressing conserved structural motifs.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"117049"},"PeriodicalIF":5.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A mathematical formalism to quantify drug-target residence time. 一种量化药物靶标停留时间的数学形式。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-12 DOI: 10.1016/j.bcp.2025.117037

Antonio J Ortiz, David Romero, Antoni Guillamon, Jesús Giraldo

{"title":"A mathematical formalism to quantify drug-target residence time.","authors":"Antonio J Ortiz, David Romero, Antoni Guillamon, Jesús Giraldo","doi":"10.1016/j.bcp.2025.117037","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.117037","url":null,"abstract":"<p><p>Despite drug-target residence time (RT) is a key topic in binding kinetics, little information exists on its theoretical quantification. The two most frequent mathematical expressions found in the literature correspond to two particular and simple pharmacological cases: the binary ligand-receptor complex and the induction-fit model. In this article, we propose a mathematical formalism to obtain an expression of RT that can be of general applicability. RT is calculated from the system of ordinary differential equations (ODE) obtained by applying the Law of Mass Action to the selected chemical process. Then, a subsystem is constructed by defining which chemical species are of interest and omitting their global formation processes. RT maintains its accepted definition of 1/k<sub>off</sub>, where k<sub>off</sub> is here defined as the absolute value of the smallest-modulus eigenvalue of the subsystem. The proposed procedure is successfully used to derive RT for a wide variety of pharmacological cases. In particular, the theoretical expressions of RT obtained for binary ligand-receptor binding and induction-fit coincide with those previously found in the literature. An extension of the RT pharmacological framework is proposed by including the concept of relaxation time (RXT), which involves pharmacological conditions associated with receptor activation rather than receptor binding. To conclude, the herein presented formalism for RT and RXT provides a mathematical framework that can be of general applicability in many pharmacological systems. It is expected that the procedure may be helpful in different pharmacological areas such as binding kinetics, PK/PD and enzymology.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"117037"},"PeriodicalIF":5.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NAD+ glycohydrolases-CD38 as a therapeutic target in aging: physiological roles, molecular mechanisms, and future opportunities in anti-aging research NAD+糖水解酶- cd38作为衰老治疗靶点：生理作用、分子机制及抗衰老研究的未来机遇

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-12 DOI: 10.1016/j.bcp.2025.117050

Jing-Yu Sun , Zhi-Fei Wang , Wen-Hui Xu, Jun Zhao

{"title":"NAD+ glycohydrolases-CD38 as a therapeutic target in aging: physiological roles, molecular mechanisms, and future opportunities in anti-aging research","authors":"Jing-Yu Sun , Zhi-Fei Wang , Wen-Hui Xu, Jun Zhao","doi":"10.1016/j.bcp.2025.117050","DOIUrl":"10.1016/j.bcp.2025.117050","url":null,"abstract":"<div><div>As individuals age, tissue homeostasis and functionality gradually deteriorate, leading to the occurrence and advancement of age-related illnesses. Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is essential for metabolism and cellular energy generation. The significance of maintaining adequate the levels of NAD<sup>+</sup> within biological systems to ameliorate age-related tissue degeneration and prevent age-related illnesses in senescent animals is now widely recognized, emphasizing the importance of increasing NAD<sup>+</sup> levels. Cluster of differentiation 38 (CD38), a multifunctional enzyme, plays a significant role in maintaining the cellular equilibrium of NAD<sup>+</sup> through the consumption of NAD<sup>+</sup>. Recent research has shown a correlation between aging and upregulation of CD38 expression, potentially resulting in a reduction in NAD<sup>+</sup> with increasing age. In contrast, the lack of CD38 has been shown to have a beneficial effect on slowing the aging process. Consequently, CD38 has been increasingly identified as a potential therapeutic target for interventions aimed at combatting aging. This study investigated the physiological roles of CD38, its ramifications in the aging process, possible molecular mechanisms associated with its involvement in aging-related diseases, and possible therapeutic applications of small-molecule inhibitors targeting CD38 in the context of aging. In this review, we provide a comprehensive analysis of the potential applications and future opportunities of CD38 in anti-aging research.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"239 ","pages":"Article 117050"},"PeriodicalIF":5.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Allosteric modulation of neurotransmission 神经传递的变构调节。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-11 DOI: 10.1016/j.bcp.2025.117026

Terry Kenakin

引用次数: 0

Retraction notice to "Comprehensive review for non-coding RNAs: From mechanisms to therapeutic applications" [Biochem. Pharmacol. 224 (2024) 116218]. 对“非编码rna综合综述：从机制到治疗应用”的撤回通知[生物化学]。药理学杂志，24(24):116218。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-10 DOI: 10.1016/j.bcp.2025.117025

YanJun Zhang, Lijuan Zhan, Xue Jiang, Xiaozhu Tang

引用次数: 0

An updated review on the inhibition of exosome biogenesis, release, and uptake: a potential anticancer approach 抑制外泌体的生物发生、释放和摄取：一种潜在的抗癌方法的最新综述。

IF 5.3 2区医学

Biochemical pharmacology Pub Date : 2025-06-09 DOI: 10.1016/j.bcp.2025.117019

Salar Ghaffari Gabaran , Vahid Nejati , Nihat Dilsiz , Jafar Rezaie

{"title":"An updated review on the inhibition of exosome biogenesis, release, and uptake: a potential anticancer approach","authors":"Salar Ghaffari Gabaran , Vahid Nejati , Nihat Dilsiz , Jafar Rezaie","doi":"10.1016/j.bcp.2025.117019","DOIUrl":"10.1016/j.bcp.2025.117019","url":null,"abstract":"<div><div>Extracellular vesicles, exosomes, have garnered significant attention in the field of cancer therapy, one of the world’s deadliest diseases. Exosomes from cancer cells participate in the development of cancer. Inhibition of exosome biogenesis may be a promising way to combat cancer. Numerous drugs and agents have been assessed to inhibit exosome biogenesis, release, and uptake, which are the main factors contributing to cancer progression. Different drugs target several intracellular mechanisms to stop the exosome signalling pathway. They affect various intracellular pathways; for example, they can disrupt the endosomal sorting complex or interfere with the intracellular trafficking of exosomes Furthermore, some of them suppress or modulate genes and proteins involved in exosome generation and release. Exosome inhibition may also be associated with different side and non-targeting effects. Pre-clinical studies show promising outcomes; however, some challenges need to be addressed in future studies. This review describes the properties of exosome inhibitor agents, focusing on the specific pathways involved in exosome biogenesis, release, and uptake.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"239 ","pages":"Article 117019"},"PeriodicalIF":5.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0