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Corrigendum to “From natural drug regulation to precise targeted intervention: Anti-heart failure mechanisms based on the reconstruction of calcium-lipid homeostasis via mitochondria-endoplasmic reticulum structural coupling” [Pharmacol. Res. (2026) 229 108259] “从天然药物调节到精确靶向干预:通过线粒体-内质网结构偶联重建钙-脂质稳态的抗心力衰竭机制”的勘误表[Pharmacol]。Res.(2026) 229[8259]。
IF 12.2 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-07-01 Epub Date: 2026-06-11 DOI: 10.1016/j.phrs.2026.108286
Qin Zhang, Yi Wei, Haijing Li, Wei Wang, Yong Wang
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引用次数: 0
Retraction notice to "PIM1 kinase inhibitors induce radiosensitization in non-small cell lung cancer cells" [Pharmacol. Res. 70 (2013) 90–101] 关于“PIM1激酶抑制剂诱导非小细胞肺癌细胞放射增敏”的撤回通知[Pharmacol]。Res. 70(2013) 90-101]。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-06-01 Epub Date: 2026-04-29 DOI: 10.1016/j.phrs.2026.108165
Wanyeon Kim , HyeSook Youn , TaeWoo Kwon , JiHoon Kang , EunGi Kim , Beomseok Son , Hee Jung Yang , Youngmi Jung , BuHyun Youn
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引用次数: 0
Nuclear receptors in metabolism and diseases: Mechanistic and therapeutic insights 代谢和疾病中的核受体:机制和治疗的见解。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-06-01 Epub Date: 2026-04-23 DOI: 10.1016/j.phrs.2026.108207
Hongbing Wang , Taosheng Chen , Huichang Bi
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引用次数: 0
Corrigendum to “Efficacy of Chinese medicine WW-1 in managing gastric atrophy and intestinal metaplasia in patients with chronic atrophic gastritis: A multicenter, randomized, double-blind, placebo-controlled trial” [Pharmacol. Res. 227 (2026) 108176] 《中药ww1治疗慢性萎缩性胃炎患者胃萎缩和肠化生的疗效:一项多中心、随机、双盲、安慰剂对照试验》的勘误表[Pharmacol]。[Res. 227(2026) 108176]。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-06-01 Epub Date: 2026-05-25 DOI: 10.1016/j.phrs.2026.108262
Yang Yang , Zongshi Qin , Sijing Du , ShuangShuang Fang , Yanjun Ma , Zhaolan Liu , Weixun Zhou , Xiuli Liu , Alfred Chin Yen Tay , Yanping Tang , Chuijie Wang , Juanpin Su , Fengbin Liu , Jin Shu , Xudong Tian , Qian Yang , Huayi Liu , Li Liu , Tao Yu , Zhenhua Li , Wei Wei
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引用次数: 0
Corrigendum to “Transplanted human striatal progenitors exhibit functional integration and modulate host circuitry in a Huntington’s disease animal model” [Pharmacol. Res. 219 (2025) 107905] “移植的人类纹状体祖细胞在亨廷顿病动物模型中表现出功能整合和调节宿主电路”的勘误表[Pharmacol]。Res. 219(2025) 107905]。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-05-01 Epub Date: 2026-04-04 DOI: 10.1016/j.phrs.2026.108182
Linda Scaramuzza , Marta Ribodino , Christian Cassarino , Marta Morrocchi , Gabriela B. Gomez Gonzalez , Roberta Parolisi , Edoardo Sozzi , Giacomo Turrini , Valentina Cerrato , Paola Conforti , Eriola Hoxha , Riccardo Tognato , Greta Galeotti , Chiara Cordiglieri , Maria Cristina Crosti , Stefano Zucca , Martina Lorenzati , Serena Bovetti , Paolo Spaiardi , Claudio de’Sperati , Annalisa Buffo
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引用次数: 0
Corrigendum to “The role of cannabinoid ligands in neurodegenerative diseases: Emerging anti-inflammatory, immunomodulation and disease-modifying perspectives” [Pharmacol. Res. 227 (2026) 108185] “大麻素配体在神经退行性疾病中的作用:新兴的抗炎、免疫调节和疾病改善观点”的勘误表[Pharmacol]。[Res. 227(2026) 108185]。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-05-01 Epub Date: 2026-04-23 DOI: 10.1016/j.phrs.2026.108206
Gabriela Mantovani Baldasso , Rodrigo Sebben Paes , Artur Graeff Moreira , Sofia Gallo Salvadori , Christian Limberger , Fiorentina Roviezzo , Raffaele Capasso , Rafael Cypriano Dutra
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引用次数: 0
Editorial: Sixty years from THC: Landscape and perspectives on the pharmacology of cannabinoids 社论:六十年的THC:大麻素药理学的景观和观点。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-05-01 Epub Date: 2026-03-24 DOI: 10.1016/j.phrs.2026.108173
Luigia Cristino, Fabricio A. Moreira, Uwe Grether
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引用次数: 0
Corrigendum to “Mitochondrial dysfunction and immunoinflammatory remodeling in heart failure: Emerging role of conceptualizationthe mtDNA–cGAS/STING axis and therapeutic opportunities” [Pharmacol. Res. 227 (2026) 108195] “心力衰竭的线粒体功能障碍和免疫炎症重塑:概念化mtDNA-cGAS/STING轴和治疗机会的新兴作用”的勘误表[Pharmacol]。Res. 227(2026) 108195]。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-05-01 Epub Date: 2026-04-21 DOI: 10.1016/j.phrs.2026.108200
Xi Zhang , Xiangchen Xia , Yanmin Zhang , Xiaomin Liu , Xiaoyu Wei , Shichuan Chen , Yuchen Song , Yicheng Chen , Jianzhong Pang , Qiang Xu , Fuyun Jia
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引用次数: 0
Targeting Acod1/itaconate in cancer therapy: Mechanisms and opportunities 靶向Acod1/衣康酸治疗癌症:机制和机遇。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-03-01 Epub Date: 2026-02-13 DOI: 10.1016/j.phrs.2026.108139
Tianlin Deng , Xiuyan Li , Shuodong Wu , Jing Kong , Xiaodong Wu
Globally, cancer claims nearly 10 million lives annually, where tumor heterogeneity, the immunosuppressive microenvironment, and therapeutic resistance constitute fundamental clinical challenges. In recent years, immunometabolic reprogramming has emerged as a cutting-edge research frontier, revealing novel mechanisms by which metabolites orchestrate immune responses. Itaconate—an immunometabolite primarily synthesized by macrophages—serves as a pivotal molecular hub bridging metabolic stress and anti-tumor immunity. This review systematically traces the evolution of itaconate from an industrial chemical to a key immunometabolite; comprehensively elucidates its dual roles (pro-tumorigenic vs. anti-tumorigenic) within the tumor microenvironment; synthesizes preclinical evidence of itaconate and its derivatives across diverse tumor systems; and consolidates emerging adjuvant therapeutic strategies targeting the Acod1/itaconate pathway. Collectively, this work aims to provide innovative immunometabolic perspectives for overcoming current barriers in cancer therapy.
在全球范围内,癌症每年夺去近1000万人的生命,其中肿瘤异质性、免疫抑制微环境和治疗耐药性构成了基本的临床挑战。近年来,免疫代谢重编程已成为一个前沿的研究前沿,揭示了代谢物协调免疫反应的新机制。itaconate是一种主要由巨噬细胞合成的免疫代谢物,是连接代谢应激和抗肿瘤免疫的关键分子枢纽。本综述系统地追溯衣康酸从工业化学品到关键免疫代谢物的演变;全面阐明其在肿瘤微环境中的双重作用(促瘤性和抗瘤性);衣康酸及其衍生物在不同肿瘤系统中的临床前证据综合;并巩固了针对Acod1/itaconate通路的新兴辅助治疗策略。总的来说,这项工作旨在为克服目前癌症治疗中的障碍提供创新的免疫代谢视角。
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引用次数: 0
Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus 长期摄入咖啡因可以通过减少神经炎症和增强海马体中的神经元活动来预防肥胖引起的认知和记忆障碍。
IF 10.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2026-03-01 Epub Date: 2026-02-13 DOI: 10.1016/j.phrs.2026.108140
Adriana M. Capucho , José Ponce de Leão , Karine Correa Flor , Gonçalo M. Melo , Marcos Vinicius Fernandes , Joana F. Sacramento , Sílvia V. Conde
Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders. Chronic caffeine consumption was suggested to prevent synaptic and cognitive deficits, but the underlying mechanisms remain unclear. Here, we investigated whether caffeine protects against cognitive and memory deficits and anxiety induced by a hypercaloric diet, and explored the molecular mechanisms involved. Ten-week-old male Wistar rats were assigned to three groups: normal chow (control), high-fat high-sucrose (HFHSu, 25 weeks), and HFHSu plus caffeine (HFHSuCaff, 1 g/L last 11 weeks). Insulin sensitivity and glucose tolerance were assessed at weeks 14 and 25. Behavioral tests (open field, novel object recognition (NOR), Y-maze, block test, elevated plus maze (EPM)) evaluated memory, cognition, and anxiety. Hippocampal tissues were analyzed by Western blot and immunohistochemistry for insulin signaling, neuronal activity and microglia activation. HFHSu feeding promoted obesity, insulin resistance, and glucose intolerance, accompanied by impaired memory and cognition (reductions in Y-maze, NOR, and block test), increased anxiety (54.5 % time in EPM open arms), reduced hippocampal glutamatergic (41.1 % VGlut) and adenosinergic signaling (22.4 %, 11.1 %, 22.6 % in A1, A2A, A2B receptors), and elevated neuroinflammation (elevated GFAP, IBA-1, IL-6 receptor levels; altered microglial morphology) compared with control. Caffeine intake ameliorated metabolic, cognitive, and neuroinflammatory alterations, except for anxiety. Notably, caffeine increased hippocampal neuronal activity by 25.22, 94.84 and 61.51 % in CA1, CA2 and CA3 areas. In conclusion, chronic caffeine consumption mitigates obesity-induced cognitive and memory deficits via modulation of hippocampal glutamatergic and adenosinergic signaling and reduced neuroinflammation, highlighting its potential as a neuroprotective intervention.
肥胖及其相关的代谢紊乱会增加认知能力下降、痴呆和焦虑相关疾病的风险。长期摄入咖啡因被认为可以预防突触和认知缺陷,但潜在的机制尚不清楚。在这里,我们研究了咖啡因是否能预防高热量饮食引起的认知、记忆缺陷和焦虑,并探讨了其中的分子机制。将10周龄雄性Wistar大鼠分为正常食物(对照组)、高脂高糖(HFHSu, 25周)和HFHSu加咖啡因(HFHSuCaff, 11周后1g/L)三组。在第14周和第25周评估胰岛素敏感性和葡萄糖耐量。行为测试(开放领域,新物体识别(NOR), y形迷宫,障碍测试,升高加迷宫(EPM))评估记忆,认知和焦虑。采用Western blot和免疫组化方法分析海马组织中胰岛素信号、神经元活性和小胶质细胞活化情况。与CTL相比,HFHSu喂养促进肥胖、胰岛素抵抗和葡萄糖耐受不良,并伴有记忆和认知功能受损(y迷宫、NOR和阻滞试验减少)、焦虑增加(EPM张开的54.5%时间)、海马谷氨酸能(41.1% VGlut)和腺苷能信号传导减少(A1、A2A、A2B受体22.4%、11.1%、22.6%)和神经炎症升高(GFAP、IBA-1、IL-6受体水平升高;小胶质细胞形态改变)。咖啡因的摄入改善了代谢、认知和神经炎症的改变,除了焦虑。值得注意的是,咖啡因使海马CA1、CA2和CA3区的神经元活性分别增加25.22%、94.84%和61.51%。综上所述,慢性咖啡因摄入通过调节海马谷氨酸能和腺苷能信号和减少神经炎症来减轻肥胖引起的认知和记忆缺陷,突出了其作为神经保护干预的潜力。
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