Current Molecular Pharmacology当代分子药理学
Current Molecular Pharmacology(英文缩写 CURR MOL PHARMACOL),ISSN 1874-4672,eISSN 1874-4702,中文译名:当代分子药理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.855 | Q2 |
| 2022 | 2.700 | Q3 |
| 2023 | 2.400 | Q3 |
| 2024 | 2.900 | Q2 |
| 2025 | 7.200 | Q1 |
Current Molecular Pharmacology 最新收录文献
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1. Sedative-hypnotic properties and mitochondrial effects of coenzyme Q2 in mice.
PMID:日期:2025-12-19Anesthetics are fascinating drugs capable of inducing reversible unconsciousness. Functional targets of these agents exist within mitochondria and disruption of bioenergetic capacity plays a role in mediating the anesthetic response. Recently, ubiquinone-5 (coenzyme Q1)(Ub5 or CoQ1), a short-chain coenzyme Q (CoQ) analog with a single isoprene unit, was identified as a novel anesthetic with a mitochondrial mechanism. Benzoquinones share an identical head group yet differ in the length of their isoprenoid tail. It is unknown if other CoQ analogs exhibit anesthetic properties or how side-chain length affects their activity. Here, we hypothesized that CoQ2, an analog with two isoprene tail units, would act as a sedative-hypnotic and that its mitochondrial biological activity would differ from Ub5 (CoQ1). Behavioral phenotype was assessed in mice using behavioral and neurophysiological approaches. We measured activity within isolated mitochondria using polarography and spectrophotometry and attempted to identify source of proton leak using pharmacological inhibitors. CoQ2 induced brief and reversible brain quiescence shortly after injection and caused a precipitous decline in the mitochondrial membrane potential due to excessive mitochondrial proton leak combined with electron transport chain inhibition. Unlike Ub5 (CoQ1), however, there was a latency to onset of CoQ2-induced hypnosis, effective CoQ2 doses were relatively higher, and duration of CoQ2-mediated unconsciousness was relatively longer than that previously reported for Ub5 (CoQ1). Furthermore, the source of proton leak differed between analogs. The comparable anesthetic effects likely relate to the benzoquinone head group shared between molecules while the disparities are likely due to the length of the isoprenoid tail.
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2. (R)-STU104 and Brefeldin-A Synergistically Enhance the Therapeutic Effect On IBD By Inhibiting the TAK1-MKK3-P38 Signaling Pathway.
PMID:日期:2024Inflammatory Bowel Disease (IBD) imposes a huge burden on both patients and the society. Standard treatments are often ineffective and can lead to adverse effects. Biological Tumor Necrosis Factor (TNF-α) inhibitors, though effective, have issues with immunogenicity and high costs. Our study investigates the potential of Brefeldin A (BFA) and (R)-STU104 in treating IBD by targeting the Transforming Growth Factor-β-Activated Kinase 1 (TAK1) - Mitogen-Activated Protein Kinase Kinase 3 (MKK3)-p38 pathway. RAW264.7 cells (Murine Leukemia macrophage cell line) were treated with (R)-STU104 and BFA to evaluate their impact on the TAK1-MKK3- p38 pathway using Western blotting and RT-qPCR. , C57BL/6 mice were given Dextran Sulfate Sodium (DSS) to induce IBD, and the effects of BFA and (R)-STU104 were assessed by monitoring Disease Activity Index (DAI), colon length, and cytokine levels. Both compounds inhibited the MKK3-p38 pathway and reduced TNF-α mRNA expression levels in a dose-dependent manner. Combination therapy showed an enhanced inhibitory effect, reducing mRNA levels of TNF-α, Interleukin (IL)-1β, and IL-6. In the DSS-induced IBD model, this combination alleviated symptoms, improved DAI scores, increased colon length, and reduced inflammatory cell infiltration. This study delved into the synergistic effect of BFA combined with (R)-STU104 on IBD treatment, and revealed that this combination can more effectively inhibit inflammatory responses, as well as enhance disease condition improvement. (R)-STU104selectively suppresses TNF-α production by targeting the p38 signaling pathway, and this suppressive effect is further strengthened when used in tandem with BFA. While,the combination therapy shows potential as an effective IBD treatment strategy,additional research is necessary to confirm its clinical applicability. BFA and (R)-STU104 exert synergistic anti-inflammatory effects by inhibiting the TAK1-MKK3-p38 pathway, suggesting a new therapeutic approach for IBD. Further studies are required to determine the clinical potential of this combination therapy.
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3. Corrigendum to: IMPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells by Activating JunB Signaling Pathway.
PMID:日期:2024An error occurred in the funding details of the manuscript titled I"MPDH2 Positively Impacts the Proliferation Potential of Hepatoblastoma Cells by Activating JunB Signaling Pathway", 2024; 17: e18761429257350 [1]. Original: This work was funded by grants from the National Natural Science Foundation of China (No. 81802346). Corrected: This work was funded by grants from the Basic Research Program of Guangzhou Science and Technology Program Project No. 202201010947. The original article can be found online at https://benthamscience.com/article/138645.
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4. Corrigendum to: An Essential Role of c-Fos in Notch1-mediated Promotion of Proliferation of KSHV-Infected SH-SY5Y Cells.
PMID:日期:2024In the online version of the article, a change was made in the author's position. The affiliation of Dongmei Li and Jinli Zhang in the online version of the article titled "An Essential Role of c-Fos in Notch1-mediated Promotion of Proliferation of KSHV-Infected SH-SY5Y Cells" has been updated in "Current Molecular Pharmacology," 2024; 17: e18761429264583 [1]. The original article can be found online at: https://www.eurekaselect.com/article/137219 Original: Huiling Xu1,2,#, Jinghong Huang1,#, Lixia Yao1,#, Wenyi Gu3, Aynisahan Ruzi4, Yufei Ding5, Ying Li6, Weihua Liang1, Jinfang Jiang1, Zemin Pan1, Dongdong Cao1, Naiming Zhou6,7,*, Dongmei Li1,# and Jinli Zhang1,# * Address correspondence to this author at the Institute of Biochemistry, College of Life Sciences, Zijingang Campus, Zhejiang University, Hangzhou, Zhejiang 310058, China; Tel: 86-13588743854; E-mail: zhounaiming@zju.edu.cn #This author has contributed equally to this work Corrected: Huiling Xu1,2,#, Jinghong Huang1,#, Lixia Yao1,#, Wenyi Gu3, Aynisahan Ruzi4, Yufei Ding5, Ying Li6, Weihua Liang1, Jinfang Jiang1, Zemin Pan1, Dongdong Cao1, Naiming Zhou6,7,*, Dongmei Li1,#,* and Jinli Zhang1,#,* * Address correspondence to these authors at the Institute of Biochemistry, College of Life Sciences, Zijingang Campus, Zhejiang University, Hangzhou, Zhejiang 310058, China. Department of Biochemistry and Molecular Biology/Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine 59 North 2nd Road, Shihezi, Xinjiang, 832002 China. Department of Biochemistry and Molecular Biology/Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine 59 North 2nd Road, Shihezi, Xinjiang, 832002 China. Tel: +86-13588743854; E-mail: zhounaiming@zju.edu.cn Tel: +86-993-2057882; E-mail: lidong_abc@126.com, lidongmei@shzu.edu.cn Tel: +86-993-2057882; E-mail: jinli1998@126.com #These authors have contributed equally to this work.
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5. Corrigendum to: Progress of Angiogenesis Signal Pathway and Antiangiogenic Drugs in Nasopharyngeal Carcinoma.
5. 鼻咽癌血管生成信号通路及抗血管生成药物研究进展的勘误PMID:日期:2024In the online version of the article titled 'Progress of Angiogenesis Signal Pathway and Antiangiogenic Drugs in Nasopharyngeal Carcinoma' published in Current Molecular Pharmacology (2024; 2: e18761429290933), a change was made in the author position. [1]. The original article can be found online at: https://www.eurekaselect.com/article/139869 Original: Yunzhi Zhu1,3,#, Yi Hu2,#, Chengsheng Yang1, Shipu Huang1, Jianping Wen4,#, Weiguo Huang1,3,# and Shengjun Xiao1,3,* Corrected: Yunzhi Zhu1,3,#, Yi Hu2,#, Chengsheng Yang1, Shipu Huang1, Jianping Wen4,*, Weiguo Huang1,3,* and Shengjun Xiao1,3,.
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6. Corrigendum to: Bedaquiline in Drug-Resistant Tuberculosis: A Mini-Review.
PMID:日期:2024In the online version of the article, a change was made in the list of author's and affiliation section. The affiliation of Charan Singh in the online version of the article titled "Bedaquiline in Drug-Resistant Tuberculosis: A Mini-Review" has been updated in "Current Molecular Pharmacology," 2023; 16: e210422203904 [1]. The original article can be found online at: https://www.eurekaselect.com/article/122759 Original: Baljinder Singh1 1Department of Pharmaceutics, UIPS, Panjab University, Chandigarh 160014, India Corrected: 1Department of Pharmaceutics, UIPS, Punjab University, Chandigarh 160014, India 2Department of Pharmaceutics, ISF College of Pharmacy, Moga, Punjab, 142001, India 3Department of Pharmaceutical Sciences, School of Sciences, Hemvati Nandan Bahuguna Garhwal University (A Central University), Srinagar, Uttarakhand, 246174, India Funding: Original: None. Corrected: The financial support provided by the Science and Engineering Research Board (SERB), Department of Science and Technology (DST), Government of India, under the Research Grant File No. EEQ/2020/000616.
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7. {"_":"Network Pharmacology and Bioinformatics of Flavonoids from : Mitigating Aβ-Induced Cognitive Impairment in Rats the MEK-ERK-CREB Pathway.","i":["Scutellaria baicalensis stems","via"]}
PMID:日期:2024This study investigates the effects and mechanisms of (SSF) on passive avoidance learning and memory deficits induced by composite amyloid-β proteins (Aβ) via the MEK-ERK-CREB signaling pathway in rats based on network pharmacology and bioinformatics. Network pharmacology and bioinformatics identified target pathways. An Alzheimer's disease model was induced in male wistar rats using Aβ, AlCl, and RHTGF-β(referred to as compound Aβ). Memory impairment was confirmed with the Morris water maze. Modeled rats were assigned to a control group and three SSF-treated groups for 33 days. Passive avoidance learning abilities were assessed with a step-down test, and p-crebser133 expression in the hippocampus was detected via immunohistochemistry. Real-time qPCR and western blotting measured mRNA and protein levels of c-Raf, MEKs, Rsk, and zif268 in the hippocampus and cortex. Pathways such as the calcium signaling pathway, Apelin signaling pathway and cAMP signaling pathway were highlighted by KEGG analysis. The model had an 83.30% success rate. Model rats showed dry coats and unresponsiveness, while SSF treatment improved appearance and behavior. In passive avoidance tests, model rats made more errors and had shorter latencies (P < 0.01). They also showed decreased p-CREBSer133 and increased c-Raf, Rsk, and P-MEKs levels (P < 0.01), with reduced Zif268 (P < 0.01). SSF reversed these effects, enhancing p-CREBSer133 and Zif268 while regulating c-Raf, Rsk, and P-MEKs (P < 0.01). SSF ameliorates learning and memory impairments induced by composite Aβ, acting through the MEK-ERK-CREB pathway in rats.
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8. Stimulation of Soluble Guanylyl Cyclase (sGC) by Cinaciguat Attenuates Sepsisinduced Cardiac Injury
8. Cinaciguat刺激可溶性鸟苷酸环化酶（sGC）可减轻败血症引起的心脏损伤PMID:日期:2024Cinaciguat is a soluble Guanylyl Cyclase (sGC) activator that plays a crucial role in cardiovascular diseases. Previous research has shown that cinaciguat is involved in the progression of cardiomyopathy, which encompasses cardiac enlargement, heart dysfunction, and doxorubicin-induced heart damage. However, its therapeutic potential in sepsis-induced cardiomyopathy remains unknown. This study examined the impact of cinaciguat on Lipopolysaccharide (LPS)-induced myocardial injury and the underlying molecular mechanisms. The mice model was established through intraperitoneal injection of LPS (10 mg/kg), and an model was generated by stimulating H9C2 cells with LPS (10 μg/ml) for 12 h. Subsequently, the sGC activator cinaciguat was used to assess its effects on LPS-induced cardiac injury. Additionally, echocardiography was conducted 12 hours after modeling to analyze cardiac function in mice. We used various methods to evaluate inflammation, and apoptosis, including Enzyme-Linked Immunosorbent Assay (ELISA), terminal deoxynucleotidyl transferase-mediated deoxyuridine Triphosphate Nick End Labeling (TUNEL) assay, Hematoxylin and Eosin (H&E) staining, western blotting and Real-Time Polymerase Chain Reaction (RT-PCR). Additionally, the protein kinase cGMP-dependent 1 (PRKG1)/cAMP-Response Element Binding protein (CREB) signaling pathway and Mitochondrial Ferritin (FtMt) in LPS-induced cardiac injury was assessed via Western blot analysis. LPS-induced cardiac dysfunction and increased levels of cardiac injury markers Cardiac Troponin T (cTnT) . This change was accompanied by an increase in inflammatory cytokines through Interleu-1β (IL-1β), Tumor Necrosis Factor α (TNF-α), and Interleu-6 (IL-6). The expression of apoptosis, such as cleaved caspase-3, Bax, and Bcl-2, was also upregulated. However, these effects were reversed via treatment with cinaciguat. Additionally, cinaciguat alleviated LPS-induced cardiac inflammation and apoptosis by activating the PRKG1/CREB signaling pathway, and promoting FtMt expression. The same results were also obtained in H9C2 cardiomyocytes. We demonstrated that cinaciguat alleviated LPS-induced cardiac dysfunction, inflammation, and apoptosis through the PRKG1/CREB/FtMt pathway, thereby protecting against LPS-induced cardiac injury. This study identified a new strategy for treating cardiac injury caused by sepsis.
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9. Direct Thrombin Inhibitors Suppress Type 1 Diabetes Development through PI3K/p-AKT Pathway.
PMID:日期:2024Diabetes mellitus type-1 is an immunological disease associated with low insulin release and hyperglycemia due to beta cell loss. No clear studies show the relationship between the coagulation cascade activation and diabetes mellitus type-1 development. The present work aimed to clarify the function of the active coagulation system in the progression of diabetes mellitus type-1 (T1DM). Furthermore, the possible protective action of direct thrombin inhibitors (dabigatran) against T1DM caused by streptozotocin (STZ)-induced T1DM in mice model was examined. Forty Balb/c male albino mice were distributed into four different groups, with 10 mice in each group: normal, dabigatran (DAB)-treated, STZtreated, and STZ+DAB. Blood glucose, blood platelets, serum insulin, nuclear consistency, and pancreas histopathological changes were evaluated. Moreover, the expressions of PI3K, p-Akt, insulin, and fibrinogen were investigated in the pancreatic tissues via immunofluorescent technique. The findings displayed enhanced islet expression of fibrinogen, p-Akt, and PI3K proteins along with thrombocytopenia in STZ-injected mice when equated to control. Furthermore, treatment with STZ reduced pancreatic insulin expression. DAB and STZ-cotreatment significantly diminished pancreatic tissue expression of fibrinogen, PI3K, and p-AKT, as well as increased platelet counts and pancreatic insulin expression. The evidence supported the activation of coagulation cascade in T1DM through the PI3K/AKT pathway. Using direct antithrombin therapy may open new avenues for T1DM prevention in high-risk diabetes individuals.
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10. {"_":"Targeting Airway Remodeling in Asthma: Anti-EMT Effects of Xuanfei Pingchuan Prescription TGFβ1/Smad Pathway Modulation.","i":["via"]}
PMID:日期:2024Asthma is a chronic airway disease characterized by Airway Remodeling (AR) and persistent inflammation, with Epithelial-Mesenchymal Transition (EMT) playing a crucial role in fibrosis and smooth muscle proliferation. The Transforming Growth Factor-Beta1 (TGFβ1)/Smad pathway is a key driver of EMT in asthma. Current treatments do not effectively prevent AR progression. Traditional Chinese Medicine, particularly the Xuanfei Pingchuan (XFPC) prescription, has shown potential in managing asthma, but its role in EMT regulation remains unclear. This study explored the role of "phlegm and stasis" in airway remodeling (AR) in asthma from the perspective of EMT and investigated the effects and underlying mechanisms of XFPC prescription on EMT in AR. , human bronchial epithelial (16HBE) cells were induced into EMT with TGFβ1 and treated with XFPC drug-containing serum, with EMT marker expression analyzed RT-qPCR and Western blot. , an ovalbumin (OVA)-induced asthma model in Sprague Dawley rats was used to evaluate the effects of different XFPC doses through histopathology, immunofluorescence, and molecular analyses. Additionally, Smurf2 cDNA transfection was conducted to assess the role of Smurf2 in EMT regulation. The results confirmed that XFPC prescription suppressed the pathway of transforming-growth factor-beta1 (TGFβ1)-Smad by reducing Smad ubiquitination regulator 2 (Smurf2), Smad2, Smad3, TGFβ1 receptor (TβRI), N-cadherin, α-SMA, and Vimentin in terms of expressions at messenger ribonucleic acid (mRNA) and protein levels. However, XFPC prescription up-regulated expressions of SnoN and E-cadherin at protein and mRNA levels to inhibit EMT. The result also confirmed that XFPC prescription decreased the ubiquitination of Smad7. XFPC prescription could suppress AR in TGFβ1 induced 16HBE cells and OVA-sensitized animal models through TGFβ1/Smad pathway.