Biochemical pharmacology最新文献

{"title":"Corrigendum to “Fisetin promotes osteoblast differentiation and osteogenesis through GSK-3β phosphorylation at Ser9 and consequent β-catenin activation, inhibiting osteoporosis” [Biochem. Pharmacol. 192 (2021) 114676]","authors":"Ilandarage Menu Neelaka Molagoda , Chang-Hee Kang , Mi-Hwa Lee , Yung Hyun Choi , Chang-Min Lee , Seungheon Lee , Gi-Young Kim","doi":"10.1016/j.bcp.2025.116956","DOIUrl":"10.1016/j.bcp.2025.116956","url":null,"abstract":"","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116956"},"PeriodicalIF":5.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887762","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}

{"title":"OTUB1 enhances fatty acid oxidation in APAP-induced liver injury by mediating ACSL5 deubiquitination","authors":"Shuyu Guo ,&nbsp;Yan Zhao ,&nbsp;Yue Wang ,&nbsp;Musen Lin ,&nbsp;Qinrong Luan ,&nbsp;Zhehao Hu ,&nbsp;Xuzi Zhao ,&nbsp;Xiaofeng Tian ,&nbsp;Zhecheng Wang ,&nbsp;Jihong Yao","doi":"10.1016/j.bcp.2025.116957","DOIUrl":"10.1016/j.bcp.2025.116957","url":null,"abstract":"<div><div>Overdosing on acetaminophen (APAP) is the primary cause of drug-induced liver injury. Recent studies have demonstrated that dysregulated lipid metabolism, particularly decreased fatty acid oxidation (FAO), is a key contributor to APAP-induced acute liver injury (AILI). OTU domain-containing ubiquitin aldehyde-binding protein 1 (OTUB1), a crucial member of the OTU deubiquitinase family, has been involved in the metabolic progression of multiple diseases. Nevertheless, its involvement in AILI as well as FAO remains unclear. Here, we aimed to elucidate the effects of OTUB1 on the regulation of FAO in AILI. Our investigation revealed decreased OTUB1 expression in AILI. OTUB1 overexpression not only alleviated liver injury but also improved FAO in vivo and in vitro. Conversely, opposite biochemical changes were observed in hepatocytes with OTUB1 knockdown. Mechanistically, long-chain acyl-CoA synthase 5 (ACSL5), which plays a crucial role in regulating FAO, was identified as a novel substrate of OTUB1 in AILI via mass spectrometry analysis. OTUB1 interacts with ACSL5 and promotes its deubiquitination and stability. Moreover, the protective effect of OTUB1 on FAO in AILI occurred via the deubiquitination of ACSL5. Overall, the present study revealed that the OTUB1-ACSL5 axis plays an essential role in regulating FAO during AILI progression and might be a novel target for therapeutic intervention.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116957"},"PeriodicalIF":5.3,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874116","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}

{"title":"Integrative CYP450 and network pharmacology approach for the assessment of Corilagin’s influence on Sitagliptin pharmacokinetics","authors":"Bhukya Siva ,&nbsp;Sahla Sherin ,&nbsp;Ravi Adinarayan Somabattni ,&nbsp;Satheesh Kumar Nanjappan","doi":"10.1016/j.bcp.2025.116960","DOIUrl":"10.1016/j.bcp.2025.116960","url":null,"abstract":"<div><div>Type 2 diabetes (T2D) is a complex metabolic disorder marked by elevated blood glucose levels and a high risk of cardiovascular complications. Sitagliptin (SIT), a widely prescribed Dipeptidyl Peptidase-4 (DPP-4) inhibitor, is commonly used for T2D and undergoes extensive metabolism primarily via CYP3A4. Corilagin (COR), a bioactive ellagitannin known for its antioxidant, anti-inflammatory, and anti-diabetic properties, is frequently used in traditional medicine but is not well-studied for its CYP450 metabolism. This study employed a network pharmacology and pharmacokinetics approach to evaluate COR’s influence on SIT. A total of 45 overlapping anti-diabetic gene targets were identified, and pathway enrichment analysis highlighted insulin resistance, lipid metabolism, and HIF-1 signalling, among others, as potential therapeutic intersections. CYP3A4 and CYP2C8 inhibition assays showed IC₅₀ values of 2.815 µM and 0.645 µM for SIT, 4.277 µM and 0.470 µM for COR, and 3.999 µM and 0.389 µM for their combination, respectively. CYP3A4 inhibition assays showed IC₅₀ values of 2.815 µM for SIT, 4.277 µM for COR, and 3.999 µM for their combination, indicating COR’s influence on SIT metabolism. These findings suggest that COR may alter SIT’s pharmacokinetic profile via CYP3A4 modulation, warranting caution in their combined use to maintain therapeutic efficacy. A sensitive LC-MS-QTOF method was developed to quantify SIT and COR in rat plasma concurrently. Pharmacokinetic analysis revealed that COR co-administration significantly reduced SIT’s bioavailability, decreasing C_max by 5.8-fold and AUC by 14.96-fold and prolonging t_1/2 by increasing 1.52-fold. This integrated approach provides insight into herb-drug interactions in diabetes treatment, emphasizing the need for tailored dosing strategies in clinical applications.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116960"},"PeriodicalIF":5.3,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881667","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}

{"title":"Identification of pyrazole scaffold inhibitors targeting cyclin-dependent kinase 8 for potential use in pulmonary fibrosis","authors":"Tony Eight Lin ,&nbsp;Kai-Cheng Hsu ,&nbsp;Ching-Hsuan Chou ,&nbsp;En-Yun Tsai ,&nbsp;Yi-Wen Wu ,&nbsp;Tzu-Ying Sung ,&nbsp;Jui-Yi Hsu ,&nbsp;Jui-Hua Hsieh ,&nbsp;Shih-Chung Yen ,&nbsp;Yu-Wei Chang ,&nbsp;Shiow-Lin Pan ,&nbsp;Wei-Jan Huang ,&nbsp;Chia-Ron Yang","doi":"10.1016/j.bcp.2025.116959","DOIUrl":"10.1016/j.bcp.2025.116959","url":null,"abstract":"<div><div>Idiopathic Pulmonary Fibrosis (IPF) is a disease that includes inflammation and scarring of the lung tissues. Cyclin-dependent kinase 8 (CDK8) is a target of interest due to its role in inflammatory pathways. CDK8 can also modulate the TGF-β/Smad signaling associated with IPF. Herein, a structure-based virtual screening (SBVS) campaign led to the identification of three CDK8 inhibitors. Testing of candidate inhibitors in protein and cellular assays confirmed CDK8 inhibition, with the most potent inhibitor producing an IC₅₀ value of 398.8 nM. Computational analysis identified pharmacological interactions that lead to CDK8 inhibition. No significant cytotoxicity was observed when the inhibitor was treated <em>in vitro</em>. Further results showed that the inhibitor can disrupt proteins associated with the epithelial-mesenchymal transition (EMT) and reduce cell migration. Additionally, the inhibitor can disrupt the TGF- β1/Smad signaling axis in the nucleus, potentially impacting the transcription of IPF related protein expression, when treated in cells at 5 µM. Comparisons to structures of known CDK8 inhibitors showed the identified inhibitor to be structurally novel. When tested against a panel of kinases at 1 µM, the most potent inhibitor demonstrated a favorable CDK8 selectivity profile. The identification of the CDK8 inhibitors in this study can be used in future drug design studies and as CDK8 probes to explore alternative therapeutics for IPF.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116959"},"PeriodicalIF":5.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881660","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}

{"title":"GSNO induced mitochondrial Cx43 nitrosylation in cardiomyocyte differentiation from mouse ES cells in vitro","authors":"Jiayu Qi ,&nbsp;Ying Shao ,&nbsp;Liting Chen ,&nbsp;Danyan Zhu","doi":"10.1016/j.bcp.2025.116955","DOIUrl":"10.1016/j.bcp.2025.116955","url":null,"abstract":"<div><div><em>S</em>-nitrosoglutathione (GSNO), considered vital to <em>S</em>-nitrosylation of proteins, has been found fundamentally important to the cardiomyocytes (CMs) maturation. Our previous studies demonstrated that GSNO treatment significantly enhanced the <em>S</em>-nitrosylation of 104 proteins during the differentiation of mouse embryonic stem cells (ESCs) into CMs. Mitochondrial Cx43 (mtCx43), a membrane protein implicated in the intercellular communication, also plays a pivotal role in CMs regeneration from stem cells. However, the involvement of mtCx43 <em>S</em>-nitrosylation in GSNO-induced myocardial differentiation has not been fully elucidated. In this study, we employed an ESCs-derived CMs differentiation model to elucidate the mechanisms underlying GSNO-induced cardiogenesis. Our findings revealed that GSNO treatment significantly up-regulated mitochondrial transmembrane potential, ATP production, reactive oxygen species (ROS) levels, respiratory chain complex Ι activity and mtCx43 hemichannel permeability in embryoid bodies (EBs). Furthermore, <em>S</em>-nitrosylation of mtCx43 was markedly enhanced in differentiating EBs after GSNO treatment. Overexpression of mtCx43 further amplified the pro-mitochondrial maturation effects of GSNO, whereas overexpression of a mutant form, mtCx43^C271A attenuated this effect. To investigate the functional role of mtCx43 hemichannels, we pretreated EBs with Gap19, a specific mtCx43 hemichannel blocker, followed by GSNO administration. Gap19 significantly reduced in mitofusin 2 (Mfn2) expression, thereby impairing mitochondrial maturation and function. In addition, Gap19 treatment abrogated the pro-cardiogenic effects of mtCx43 <em>S</em>-nitrosylation. Furthermore, we demonstrated that mtCx43 <em>S</em>-nitrosylation-induced cardiac differentiation was dependent on mitochondrial Ca²⁺ uptake. In conclusion, GSNO-induced <em>S</em>-nitrosylation of mtCx43 enhances mitochondrial function in EBs by promoting the opening of mtCx43 hemichannels, thus facilitating the targeted differentiation of ESCs into CMs. These findings provide novel insights into the role of mtCx43 <em>S</em>-nitrosylation in mitochondrial regulation and cardiac lineage commitment.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116955"},"PeriodicalIF":5.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143876577","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}

{"title":"The roles of bacteria on urolithiasis progression and associated compounds","authors":"Huifang Li ,&nbsp;Xiaoyan Xue ,&nbsp;Guangxing Meng ,&nbsp;Chengwu He ,&nbsp;Lingfei Tong ,&nbsp;Yongchang Lai","doi":"10.1016/j.bcp.2025.116958","DOIUrl":"10.1016/j.bcp.2025.116958","url":null,"abstract":"<div><div>As a common urological disease, the formation of urinary tract stones involves multiple factors, including genetics, the environment, dietary habits, and bacterial species (e.g., <em>Proteus mirabilis</em> and <em>Escherichia coli</em>). Previous studies have demonstrated that <em>P. mirabilis</em> primarily contributes to infectious urinary calculus formation by producing urease, an enzyme that breaks down urea into ammonia and carbon dioxide, thereby altering the urinary pH and promoting crystal formation and growth. In contrast, calcium oxalate (CaOx) stones are the main type of kidney stones, and the most common bacteria in CaOx stones are <em>E. coli</em>. Intriguingly, <em>E. coli</em> can also facilitate stone formation via flagellin and other virulence factors, which induce renal epithelial cell injury and increase crystal adhesion and aggregation. These bacteria play complex and multidimensional roles in the formation of urinary tract stones, necessitating further research to elucidate their underlying mechanisms. Here, we summarise the roles of common urinary tract bacteria, particularly <em>P. mirabilis</em> and <em>E. coli</em>, in forming urinary tract stones, aiming to enhance our understanding of urolithiasis exploration in the future.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116958"},"PeriodicalIF":5.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870753","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}

{"title":"Sphingosylphosphorylcholine induces itch via activation of TRPM3 and TRPA1 in mice","authors":"Da Eun Song ,&nbsp;Diwas Rawal ,&nbsp;Wook-Joo Lee ,&nbsp;Won-Sik Shim","doi":"10.1016/j.bcp.2025.116952","DOIUrl":"10.1016/j.bcp.2025.116952","url":null,"abstract":"<div><div>Itch is a prevalent symptom in atopic dermatitis (AD), often leading to a strong urge to scratch. Elevated levels of sphingosylphosphorylcholine (SPC) are found in the stratum corneum of AD patients, and while SPC is known to induce itch, its molecular targets are not well understood. This study aims to identify the signaling pathway of SPC-induced itch under AD conditions. We demonstrate that SPC specifically activates the Transient Receptor Potential Melastatin 3 (TRPM3) channel in sensory neurons. In HEK293T cells expressing TRPM3, SPC treatment caused a significant increase in intracellular calcium, which was inhibited by TRPM3 antagonists. Among various TRP channels tested, TRPM3 exhibited the highest reactivity to SPC, followed by TRPA1. Molecular docking analysis also supported interactions between SPC and both TRPM3 and TRPA1. In an AD mouse model, SPC-induced responses were dependent on TRPM3 and TRPA1, and the expression of these channels increased in dorsal root ganglion neurons. SPC-induced scratching behaviors were significantly reduced by TRPM3 and TRPA1 antagonists, with TRPM3 playing a critical role in spontaneous scratching. This study identifies TRPM3 and TRPA1 as key mediators of SPC-induced itch, providing potential therapeutic targets for treating itch in AD patients.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116952"},"PeriodicalIF":5.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870752","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}

{"title":"Necroptosis: a significant and promising target for intervention of cardiovascular disease","authors":"Yan-wei Ji ,&nbsp;Xin-yu Wen ,&nbsp;He-peng Tang ,&nbsp;Wa-ting Su,&nbsp;Zhong-yuan Xia,&nbsp;Shao-qing Lei","doi":"10.1016/j.bcp.2025.116951","DOIUrl":"10.1016/j.bcp.2025.116951","url":null,"abstract":"<div><div>Due to changes in dietary structures, population aging, and the exacerbation of metabolic risk factors, the incidence of cardiovascular disease continues to rise annually, posing a significant health burden worldwide. Cell death plays a crucial role in the onset and progression of cardiovascular diseases. As a regulated endpoint encountered by cells under adverse stress conditions, the execution of necroptosis is regulated by classicalpathways, the calmodulin-dependent protein kinases (CaMK) pathway, and mitochondria-dependent pathways, and implicated in various cardiovascular diseases, including atherosclerosis, myocardial infarction, myocardial ischemia–reperfusion injury (IRI), heart failure, diabetic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, chemotherapy drug-induced cardiomyopathy, and abdominal aortic aneurysm (AAA). To further investigate potential therapeutic targets for cardiovascular diseases, we also analyzed the main molecules and their inhibitors involved in necroptosis in an effort to uncover insights for treatment.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116951"},"PeriodicalIF":5.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865058","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}

{"title":"Neutralization of IL-33 ameliorates septic myocardial injury through anti-inflammatory, anti-oxidative, and anti-apoptotic by regulating the NF-κB/STAT3/SOCS3 signaling pathway","authors":"Danlei Weng ,&nbsp;Wei Shi ,&nbsp;Yue Hu ,&nbsp;Yanqian Su ,&nbsp;Andong Li ,&nbsp;Shuxing Wei ,&nbsp;Shubin Guo","doi":"10.1016/j.bcp.2025.116954","DOIUrl":"10.1016/j.bcp.2025.116954","url":null,"abstract":"<div><div>Septic myocardial injury, a severe sepsis complication linked to high morbidity and mortality, remains a major global clinical challenge. Interleukin-33 (IL-33), a damage-associated pro-inflammatory factor, has been implicated in regulating immune responses and inflammation, but its specific role in septic myocardial injury has not been fully elucidated. This study examined IL-33’s role in septic myocardial injury using Gene Expression Omnibus (GEO) database datasets, alongside in vitro and in vivo experiments. Our results indicated a significant upregulation of IL-33 in septic myocardial injury, as demonstrated in both clinical and experimental settings. Blocking IL-33 significantly enhanced cardiac function and alleviated cardiomyocyte damage. Mechanistic investigations revealed that neutralizing IL-33 mitigates inflammation, oxidative stress, and apoptosis in cardiomyocytes by regulating the nuclear factor kappa B (NF-κB)/signal transducer and activator of transcription 3 (STAT3)/suppressors of cytokine signaling 3 (SOCS3) signaling pathway. Peritoneal macrophages are recognized as a potential origin of IL-33, and targeting IL-33 derived from these cells further reduced cardiomyocyte injury. The study underscores IL-33’s crucial involvement in septic myocardial injury pathogenesis, indicating that IL-33 may serve as a promising therapeutic target.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116954"},"PeriodicalIF":5.3,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865060","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}

{"title":"Oridonin combined with cisplatin synergistically induces apoptosis by activating the NOXA-BCL2 axis in esophageal squamous cell carcinoma","authors":"Qihang Guo ,&nbsp;Yue Mao ,&nbsp;Jiyu Zhang ,&nbsp;Yangyang Zhou ,&nbsp;Yue Zhao ,&nbsp;Ying Li ,&nbsp;Jinglong Lv ,&nbsp;Huiyu Yang ,&nbsp;Bingrong Liu","doi":"10.1016/j.bcp.2025.116953","DOIUrl":"10.1016/j.bcp.2025.116953","url":null,"abstract":"<div><div>Esophageal cancer, a malignant neoplasm originating from the epithelial cells of the esophagus, predominantly manifests as esophageal squamous cell carcinoma (ESCC) in approximately 90% of cases in China. Cisplatin-based chemotherapy regimens remain the first-line therapeutic option for ESCC, however, the five-year overall survival rate of patients is disappointingly low. Oridonin, a bioactive diterpenoid extracted from the traditional Chinese medicine herb Donglingcao, has demonstrated inhibitory effects against various malignancies. Currently, research on the combination of oridonin and cisplatin for the treatment of ESCC is limited. This study aims to elucidate the potential synergistic anti-cancer effects of oridonin in combination with cisplatin on ESCC, along with the underlying synergistic molecular mechanisms. In vitro experiments revealed that the combination of oridonin and cisplatin could synergistically inhibit ESCC cell proliferation, migration, invasion. The synergistic effect also induced cell cycle arrest and promoted apoptosis via the mitochondrial pathway by augmenting <em>NOXA</em> transcriptional activity and activating the <em>NOXA-BCL2</em> axis. In vivo experiments corroborated these findings, showing a marked reduction in the growth of subcutaneous xenograft tumors in mice treated with the combination, without exacerbating the cisplatin-associated side effects such as weight loss or hepatic and renal toxicity. In conclusion, the combination of oridonin and cisplatin can synergistically inhibit the development of ESCC through the activation of the <em>NOXA-BCL2</em> axis signaling pathway. This treatment is both safe and effective,<!--> <!-->presenting a promising prospect for combined therapeutic application in ESCC management.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"237 ","pages":"Article 116953"},"PeriodicalIF":5.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865059","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}