Biochemical pharmacology最新文献

{"title":"Metformin exhibits inhibitory effects on ferroptosis and alleviates chondrocyte metabolic imbalance in osteoarthritis models, as well as Erastin-induced ferroptosis, through the modulation of the P53/SLC7A11 pathway","authors":"Fan Jiaxin ,&nbsp;Jia Xiang ,&nbsp;Cui YongPing ,&nbsp;Liu Kainan ,&nbsp;Xu Tianjie ,&nbsp;Zhang Hui ,&nbsp;Si Shiqing ,&nbsp;Yanhua Cao ,&nbsp;Wang Qian","doi":"10.1016/j.bcp.2025.116978","DOIUrl":"10.1016/j.bcp.2025.116978","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a prevalent degenerative disease, and metformin, the first-line treatment for type 2 diabetes, has shown potential in slowing the progression of OA, although its mechanism of action is not fully understood. This study aims to explore the role of ferroptosis in OA and evaluate the therapeutic effects and mechanisms of metformin on ferroptosis. We identified gene differences associated with OA through RNA-Seq data analysis and predicted potential targets using network pharmacology and molecular docking techniques. In vivo experimental methods, including histological examination, immunofluorescence, Western blotting, real-time quantitative PCR, biochemical analysis, and ELISA, were used to study the effects of metformin in the modified Hulth method and Erastin-induced OA models. The study found that metformin significantly inhibits chondrocyte ferroptosis by upregulating SLC7A11 and downregulating P53 expression, maintaining the balance of synthesis and catabolism in chondrocytes, and effectively slowing down the degeneration of knee joint cartilage in rats. Overall, this study not only provides further evidence for the anti-OA effects of metformin but also identifies its direct targets in the inhibition of ferroptosis in OA.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116978"},"PeriodicalIF":5.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092321","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":"Inhibition of PCSK9 with polypurine reverse hoogsteen hairpins: A novel gene therapy approach","authors":"Ester López-Aguilar ,&nbsp;Silvia Cecilia Pacheco-Velázquez ,&nbsp;M-Antonia Busquets ,&nbsp;Joshua Hay ,&nbsp;Paul A. Mueller ,&nbsp;Sergio Fazio ,&nbsp;Carlos J Ciudad ,&nbsp;Véronique Noé ,&nbsp;Nathalie Pamir","doi":"10.1016/j.bcp.2025.116976","DOIUrl":"10.1016/j.bcp.2025.116976","url":null,"abstract":"<div><div>PCSK9 is a therapeutic target for hypercholesterolemia. Though different strategies to inhibit PCSK9, such as monoclonal antibodies, small molecules, or nucleic acid drugs are available, the need for safer and inexpensive interventions remains. We developed a time-, cost-, and resource- efficient silencing system using Polypurine Reverse Hoogsteen (PPRH) hairpins to target <em>PCSK9</em>. To achieve <em>PCSK9</em> silencing, we designed two PPRHs targeting <em>PCSK9</em> at exon 9 (HpE9) and exon 12 (HpE12). The binding capabilities of PPRHs were measured by EMSA: <em>K</em>_d values were 7.86 x 10^-8 M and 7.58 x 10^-7 M for HpE9 and HpE12, respectively. PPRHs were complexed with the cationic polymer jetPEI forming particles of 167 nm as characterized by Dynamic Light Scattering. <em>PCSK9</em> gene and protein expression was evaluated upon transfections of HepG2 cells with HpE9 and HpE12. PPRHs effectively reduced PCSK9 mRNA levels (63 % and 74 % for HpE9 and HpE12, respectively) and protein (by 76 % and 87 %) at 24 h. Human PCSK9 overexpressing mice receiving a single injection of HpE12 decreased plasma PCSK9 levels by 50 % by day three post injection and levels returned to baseline by day fifteen. Plasma cholesterol levels were reduced by 47 % by day three. Mice receiving the PPRHs did not exhibit changes in body weight, liver enzymes or pro-inflammatory markers when compared to mice injected with jetPEI alone. Therefore, the PPRH technology emerges as an innovative nucleic acid based therapeutic approach that is effective, cost-efficient and easy to develop, for the inhibition of PCSK9.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116976"},"PeriodicalIF":5.3,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943340","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":"In vitro pharmacological evaluation of the novel NOP receptor partial agonist sunobinop","authors":"Riccardo Camilotto ,&nbsp;Davide Malfacini ,&nbsp;Pietro Pola ,&nbsp;Erika Morrone ,&nbsp;Alessia Frezza ,&nbsp;Rahul Ramalingam ,&nbsp;Chiara Sturaro ,&nbsp;Salvatore Pacifico ,&nbsp;Chiara Ruzza ,&nbsp;Remo Guerrini ,&nbsp;Garth Whiteside ,&nbsp;Girolamo Calo’","doi":"10.1016/j.bcp.2025.116972","DOIUrl":"10.1016/j.bcp.2025.116972","url":null,"abstract":"<div><div>Sleep-related disorders affect a significant portion of the global population. The nociceptin/orphanin FQ (N/OFQ) peptide (NOP) receptor has become a promising candidate for the development of innovative drugs to treat sleep disorders. In this study, we conducted an in-depth pharmacological characterization of sunobinop, a selective NOP receptor partial agonist already under clinical evaluation for treating multiple conditions including insomnia, using a wide range of in vitro and ex vivo methodologies. Sunobinop exhibited partial agonist activity in calcium mobilization, NOP − G protein interaction, label-free bioimpedance, and cAMP inhibition assays. Notably, it demonstrated competitive antagonism in the NOP – β-Arrestin 2 recruitment and ex vivo electrically stimulated mouse Vas Deferens, assays characterized by low amplification. The findings reported here confirm and extend the characterization of sunobinop as a tool for studying NOP receptor pharmacology providing new insights into its mode of action, relevant to its clinical evaluation.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116972"},"PeriodicalIF":5.3,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967002","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":"Cholesterol metabolism: A strategy for overcoming drug resistance in tumors","authors":"Jiahui Li ,&nbsp;Yinping Guo ,&nbsp;Wenjie Zhang ,&nbsp;Min Xia ,&nbsp;Gaohua Liu ,&nbsp;Yan Sun ,&nbsp;Chang Liu ,&nbsp;Jing Zhong","doi":"10.1016/j.bcp.2025.116974","DOIUrl":"10.1016/j.bcp.2025.116974","url":null,"abstract":"<div><div>Despite significant advancements in targeted tumor therapies, the emergence of drug resistance remains a complex challenge. Cholesterol accumulation within tumor cells plays a crucial role in mediating drug resistance through various mechanisms, including altered membrane dynamics, enhanced drug efflux, and activation of survival signaling pathways. Targeting cholesterol metabolism presents an innovative strategy to enhance therapeutic sensitivity, particularly in breast cancer. Consequently, ongoing preclinical studies and clinical trials involving cholesterol-lowering agents indicate a promising direction for improving treatment outcomes in tumors. The combination of these agents with existing therapeutic regimens may lead to enhanced efficacy, highlighting the necessity for continued research in this vital area. This review examines the impact of cholesterol metabolism on drug resistance in tumors, particularly solid tumors, identifies therapeutic targets in this metabolic pathway (with a special focus on breast cancer), and discusses recent advances in cholesterol-lowering drugs in preclinical, as well as those that have entered clinical trials.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116974"},"PeriodicalIF":5.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931663","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":"Coagulin-L alleviates hepatic stellate cells activation and angiogenesis through modulation of the PI3K/AKT pathway during liver fibrosis","authors":"Abhishek Nirwan ,&nbsp;Deepika Saini ,&nbsp;Jaspreet kaur ,&nbsp;Abinash Swain ,&nbsp;Abhisek Sarkar ,&nbsp;Prem Prakash Yadav ,&nbsp;Durga Prasad Mishra","doi":"10.1016/j.bcp.2025.116979","DOIUrl":"10.1016/j.bcp.2025.116979","url":null,"abstract":"<div><div>Fibrosis, a wound healing response in chronic liver diseases, is a potential therapeutic target during the disease progression. The activation of hepatic stellate cells (HSCs) plays a central role in liver fibrosis and depicts phenotypic change during fibrosis progression. Coagulin-L, a withanolide from <em>Withania coagulans</em>, has shown diverse biological activities, including anti-hyperglycemic and anti-dyslipidemic effects. However, its therapeutic efficacy against HSC activation, pathological angiogenesis and liver fibrosis is unknown.</div><div>This study investigates the effects of Coagulin-L on HSC activation, pathological angiogenesis and validates these findings in vivo using a methionine and choline-deficient (MCD) diet-induced liver fibrosis model in C57BL/6 mice.</div><div>Therapeutic efficacy of Coagulin-L was studied using transforming growth factor beta (TGF-β) activated HSC cell line LX-2 in vitro. Network pharmacology was used for target prediction, followed by Human umbilical vein endothelial cells (HUVEC) cell based angiogenic assays. The validation studies were carried out in a mice model of MCD diet induced liver fibrosis using serum biochemistry, histopathological assessment and immunohistochemistry methods.</div><div>We found that Coagulin-L mitigated TGF-β induced activation of stellate cells and exhibited anti-angiogenic effects by downregulation of vascular endothelial growth factor (VEGF) expression and secretion from stellate cells with inhibition of the PI3K/AKT signaling pathway. In the MCD diet-induced liver fibrosis model, Coagulin-L alleviated liver injury, improved liver function, and reduced collagen deposition.</div><div>Collectively, our results underscored the anti-fibrotic and anti-angiogenic effects of Coagulin-L in vitro and in vivo liver fibrosis models, thereby indicating its therapeutic potential in chronic liver diseases including metabolic dysfunctional-associated steatohepatitis (MASH).</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116979"},"PeriodicalIF":5.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931674","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":"From stem cells to skin: ADSCP6 peptide’s role in transforming scar therapy","authors":"Jun Li ,&nbsp;Siqi Zeng ,&nbsp;Beibei Zhou ,&nbsp;Qiyue Yan ,&nbsp;Yue Sun ,&nbsp;Ling Chen ,&nbsp;Enyuan Zhang ,&nbsp;Jingyun Li","doi":"10.1016/j.bcp.2025.116980","DOIUrl":"10.1016/j.bcp.2025.116980","url":null,"abstract":"<div><div>Hypertrophic scars, caused by abnormal wound healing after injury, involve excessive fibroblast activity, ECM dysregulation, and inflammation. Bioactive peptides show antifibrotic potential. Based on our previous discovery of scar-modulating peptides from adipose-derived stem cells, this study reveals how ADSCP6 (Adipose-derived stem cell peptide 6) suppresses hypertrophic scarring. <em>In vitro</em> analyses revealed that ADSCP6 significantly downregulated type I collagen and ACTA2 (alpha smooth muscle actin) expression in human hypertrophic scar fibroblasts (HSFs), without altering proliferative/apoptotic activity. <em>In vivo</em>, topical ADSCP6 administration enhanced wound healing and attenuated collagen content in a murine excisional wound model. Transcriptomic profiling (RNA-seq) identified 328 differentially expressed genes (182 upregulated, 146 downregulated) post-treatment, with KEGG (kyoto encyclopedia of genes and genomes) pathway enrichment implicating NF-κB (nuclear factor kappa-B) signaling as a primary mechanism. Protein interaction assays (pull-down/cellular thermal shift assays) identified KANK2 (KN motif and ankyrin repeat domains 2) and ADGRE2/EMR2 (adhesion G protein-coupled receptor E2) as ADSCP6-binding partners, while western blot confirmed NF-κB1 (p50) upregulation. Functional validation demonstrated that NF-κB pathway blockade abrogated ADSCP6′s antifibrotic effects. ADSCP6 reduced the expression of FAK, STAT3, and SMAD2 proteins. Macrophage-conditioned media from ADSCP6-treated cultures suppressed HSFs collagen synthesis, and ADSCP6 significantly enhanced HUVEC (human umbilical vein endothelial cells) tubulogenesis, suggesting pro-angiogenic activity. Overall, these findings establish ADSCP6 as a multifunctional therapeutic peptide that concurrently attenuates fibrotic progression and accelerates wound healing, positioning it as a novel candidate for clinical scar management.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116980"},"PeriodicalIF":5.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931673","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":"Fatty acid synthase inhibition offers protection against pressure-induced cardiac hypertrophy","authors":"Pragya Bharati ,&nbsp;Prabha Burman ,&nbsp;Satyapriya Mahapatra ,&nbsp;Smita Prajapati ,&nbsp;Nilesh Khandelwal ,&nbsp;Baisakhi Moharana ,&nbsp;Anil Nilkanth Gaikwad ,&nbsp;Kumaravelu Jagavelu ,&nbsp;Kashif Hanif","doi":"10.1016/j.bcp.2025.116962","DOIUrl":"10.1016/j.bcp.2025.116962","url":null,"abstract":"<div><div>Disturbed cardiac metabolism is an important aspect of the pathology of Cardiac hypertrophy (CH) which precede Heart failure (HF). Studies have shown a higher rate of <em>De novo</em> lipogenesis in HF and its inhibition has been protective. However, its role in CH still needs further clarification. For <em>in vitro</em> studies, Phenylephrine (PE) was used to induce CH in adult human ventricular cardiomyocytes (AC16). For <em>in vivo</em> studies, 2 kidney 1 clip (2K1C) and Transverse aortic constriction (TAC) models of rat were used. Fatty acid synthase (FAS), key enzyme of lipogenesis was inhibited using FAS si RNA (30 nM) and C75 (2 mg/kg, i.p. once a week for 8 weeks) <em>in vitro</em> and <em>in vivo</em> respectively. Echocardiography and histochemical staining were used to observe cardiac remodeling. Western blotting, Seahorse analysis, fluorescence microscopy and FACS were performed to detect metabolic alterations, mitochondrial dysfunction, protein synthesis and hypertrophy. We observed increased expression and activity of FAS in PE-exposed AC16 and 2K1C and TAC models of rats. Inhibition of FAS decreased hypertrophy, protein synthesis by malonylation of mTOR, apoptosis, glycolysis, and oxidative stress and restored oxidative phosphorylation in AC16 cells. In rats, FAS inhibition prevented cardiac remodelling in 2K1C and TAC models. It also increased ATP, restored mitochondrial ROS and membrane potential in the TAC model of rats. Our results demonstrated that FAS activity was modulated during CH, and inhibiting it prevented cardiac remodelling and mitochondrial dysfunctions. The findings, therefore, suggest that inhibiting FAS may be a new therapeutic approach to treating CH patients.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116962"},"PeriodicalIF":5.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975909","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":"Charged dendrimers reduce glioblastoma viability by modulating lysosomal activity and HMGB1-RAGE interaction","authors":"Natali Joma ,&nbsp;Marten Kagelmacher ,&nbsp;Issan Zhang ,&nbsp;Andreas Herrmann ,&nbsp;Jens Dernedde ,&nbsp;Rainer Haag ,&nbsp;Dusica Maysinger","doi":"10.1016/j.bcp.2025.116969","DOIUrl":"10.1016/j.bcp.2025.116969","url":null,"abstract":"<div><div>Dendrimers and dendrimer-based self-assembly systems have emerged as promising nanocarriers for a variety of applications, including anti-cancer therapies, modulation of the tumor microenvironment, and imaging. Here, we explored the therapeutic potential of two charged dendrimers, dendritic polyglycerol sulfate (dPGS) and dendritic polyglycerol amine (dPGA), in the context of glioblastoma multiforme (GBM). Docosahexaenoic acid (DHA) has shown potential in GBM. We therefore examined dPGS and dPGA effects alone and in combination with DHA. Using 2D cell models and 3D tumoroids, we showed that DHA with dPGA reduced tumor integrity and cell viability. dPGS reduced oxidative stress, whereas dPGA reduced lysosomal acidification, contributing to cellular dysfunction. Both dendrimers influence the interaction between high mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE). The surfaces of the HMGB1-RAGE complex provide binding sites for interactions of charged molecules like dPGS and dPGA, suggesting the contribution of these interactions to cytotoxicity. In summary, our findings show that combining DHA with charged dendrimers (dPGS and dPGA) enhances GBM cytotoxicity through several mechanisms, involving lysosomal alkalinization, lipid peroxidation and modulation of the HMGB1-RAGE complex.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116969"},"PeriodicalIF":5.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943341","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":"Aspirin reverses the inhibitory effect of soluble fms-like tyrosine kinase-1 on trophoblast invasiveness and ciliogenesis through Sonic hedgehog signaling in preeclampsia","authors":"Yu-Jen Chen ,&nbsp;Chih-I Lee ,&nbsp;Pei-Yin Tsai ,&nbsp;Hoi-Lam Tam ,&nbsp;Mei-Tsz Su","doi":"10.1016/j.bcp.2025.116975","DOIUrl":"10.1016/j.bcp.2025.116975","url":null,"abstract":"<div><div>Soluble Flt-1 (sFlt-1) is upregulated in preeclamptic patients and is a predictive biomarker for preeclampsia risk and progression. Aspirin is an effective agent used to prevent preeclampsia and has been shown to suppress sFlt-1 production in trophoblasts; however, the underlying mechanism is not fully understood. Here, we demonstrated that sFlt-1 production was upregulated under hypoxia in two trophoblastic cells (HTR-8/SVneo and JAR). The effects of sFlt-1 and underlying pathways on trophoblast biology and cilia formation were investigated in sFlt-1-pretreated, FLT-1-knockdown HTR-8/SVneo cells under hypoxic conditions and in a preeclampsia mouse model. In the present study, sFlt-1 was shown to inhibit trophoblast invasion and migration under hypoxia, and this inhibitory effect occurred through downregulating ZEB1/2, MMP 2/9, and the Sonic hedgehog (SHH) signaling pathway. Ciliary number and length of trophoblasts were inhibited by sFlt-1 treatment and were enhanced after FLT-1 knockdown. Aspirin was found to reverse the sFlt-1-mediated inhibitory effect on trophoblast invasion/migration, ciliogenesis, and SHH signaling in HTR-8/SVneo cells. Moreover, plasma and placental sFlt-1 protein levels were upregulated in the preeclampsia mouse model, whereas primary cilia formation and SHH-related expression were impaired in the mouse placenta. Aspirin-fed mice presented with reduced sFlt-1 expression, and their placental ciliogenesis and SHH expression were improved in the preeclamptic mouse model. In conclusion, sFlt-1 impairs trophoblast motility and ciliogenesis through SHH signaling under hypoxia. Aspirin exerts its suppressive effect on sFlt-1 upregulation and sFlt-1-mediated cell function and signaling in vitro and in vivo.</div></div>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116975"},"PeriodicalIF":5.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143917268","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":"Corrigendum to “Oridonin combined with cisplatin synergistically induces apoptosis by activating the NOXA-BCL2 axis in esophageal squamous cell carcinoma” [Biochem. Pharmacol. 237 (2025) 116953]","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.2025.116965","DOIUrl":"10.1016/j.bcp.2025.116965","url":null,"abstract":"","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"238 ","pages":"Article 116965"},"PeriodicalIF":5.3,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906014","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}