European journal of pharmacology最新文献

{"title":"Copper induces antitumor immune responses by triggering cuproptosis and immunogenic cell death","authors":"Jieqi Chen,&nbsp;Mingxuan Xie,&nbsp;Zhen Yu,&nbsp;Lei Cao,&nbsp;Yue Shen,&nbsp;Xiangping Li,&nbsp;Yueqin Li","doi":"10.1016/j.ejphar.2026.179166","DOIUrl":"10.1016/j.ejphar.2026.179166","url":null,"abstract":"<div><div>Immunotherapy has improved the treatment of non-small cell lung cancer (NSCLC), but its efficacy remains limited by the immunosuppressive tumor microenvironment. Although copper has recently emerged as a potential anticancer target, its role in tumor immunity remains unclear. In this study, we investigated the effects of Cu²⁺ on tumor immunity and its impact on PD-L1 blockade therapy. Cu²⁺ significantly inhibited NSCLC growth in vitro and in vivo without causing obvious systemic toxicity. Mechanistically, Cu²⁺ induced cuproptosis, accompanied by metabolic alterations and cuproptosis-associated molecular changes. Importantly, Cu²⁺ treatment triggered immunogenic cell death (ICD), as evidenced by increased calreticulin exposure and enhanced ATP and HMGB1 release. Pharmacological inhibition of cuproptosis attenuated these ICD-associated responses, supporting a mechanistic link between cuproptosis and ICD. In vivo, Cu²⁺ treatment promoted dendritic cell maturation, increased CD4⁺ and CD8⁺ T-cell infiltration, reduced myeloid-derived suppressor cell accumulation, and facilitated macrophage polarization toward a pro-inflammatory phenotype. Furthermore, Cu²⁺ significantly enhanced the antitumor efficacy of PD-L1 blockade. These findings demonstrate that Cu²⁺ promotes antitumor immunity through a cuproptosis-associated ICD pathway and improves responsiveness to PD-L1 blockade. Targeting copper homeostasis may represent a potential strategy for enhancing immunotherapy efficacy in NSCLC.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179166"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liquiritigenin attenuates aneurysm progression and local inflammatory activation in a rabbit common carotid artery aneurysm model","authors":"Jingsong Xu,&nbsp;Yanxia Lyu,&nbsp;Haodong Liu,&nbsp;Yahui Zhang,&nbsp;Yi Zhou,&nbsp;Anrong Li,&nbsp;Zejun Wu,&nbsp;Junshuang Zhao,&nbsp;Hui Wang,&nbsp;Juntao Hu","doi":"10.1016/j.ejphar.2026.179162","DOIUrl":"10.1016/j.ejphar.2026.179162","url":null,"abstract":"<div><div>Intracranial aneurysms (IAs) are life-threatening vascular lesions closely associated with chronic inflammation in the local microenvironment. This study investigated the regulatory effect of liquiritigenin (LG), a natural flavonoid with anti-inflammatory properties, on aneurysm-associated inflammatory and vascular remodeling responses, with emphasis on HMGB1-related inflammatory signaling. Using a rabbit common carotid artery aneurysm model, we assessed the impact of liquiritigenin on inflammatory markers through histology, immunofluorescence, qPCR, and Western blot analysis. The results showed that aneurysm formation was accompanied by enhanced local inflammatory activation and increased expression of inflammation- and angiogenesis-related markers, including HMGB1, TLR4, IL-6, TREM1, TNF-α, and VEGF. Liquiritigenin treatment reduced aneurysm diameter, alleviated vessel wall pathology, and attenuated the local expression of several inflammatory and angiogenic markers. Furthermore, spatial analysis revealed heterogeneous inflammatory responses within the aneurysmal wall, suggesting the presence of localized inflammatory hotspots. In conclusion, liquiritigenin attenuates aneurysm progression in a rabbit carotid artery aneurysm model, at least in part, by modulating the local inflammatory microenvironment. These findings support liquiritigenin as a potential adjunctive pharmacological candidate for stabilizing aneurysmal vascular lesions by targeting inflammatory dysregulation.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179162"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypericin: A potential gut microbiota-based therapeutic for postpartum depression via modulating bile acid metabolism","authors":"Xin Zeng,&nbsp;Yuanmeng Zhao,&nbsp;Bin Deng,&nbsp;Yongning Lu,&nbsp;Huifan Yu,&nbsp;Qiuyun You,&nbsp;Xuejia Zhai","doi":"10.1016/j.ejphar.2026.179114","DOIUrl":"10.1016/j.ejphar.2026.179114","url":null,"abstract":"<div><h3>Background</h3><div>Postpartum depression (PPD) is a mental disorder that occurs in a special period of time, but its pathophysiological mechanism is still unclear. Although hypericin has been shown to have therapeutic effects in previous studies, the underlying mechanisms of its treatment of PPD, especially its interaction with the gut-brain axis, remain to be explored. The aim of this study was to investigate the mechanism of hypericin in the treatment of PPD.</div></div><div><h3>Methods</h3><div>The PPD rat model was established by ovariectomy and hormone withdrawal after simulating pregnancy. Postpartum depression-like behavior was assessed by sucrose preference test and open field test. We integrated 16S rRNA sequencing, targeted plasma bile acid metabolomics, brain tissue transcriptomics, histopathology and molecular biology to explain the mechanism.</div></div><div><h3>Results</h3><div>Hypericin intervention significantly improved the postpartum depression-like behavior of PPD model rats. This effect was abolished by depletion of the microbiota induced by antibiotic sweeps, thus establishing that the involvement of the gut microbiota is required for the efficacy of hypericin. Hypericin can reverse the abnormal changes of gut microbiota, bile acid metabolism and inflammatory response observed in PPD model, so as to play a role in the treatment of PPD.</div></div><div><h3>Conclusion</h3><div>Hypericin plays an antidepressant role in PPD model, mainly by restoring gut microbiota homeostasis, thereby correcting bile acid metabolism disorders. In this study, the “gut microbiota-bile acid” axis is the key pathological feature and therapeutic target of PPD, and hypericin is expected to become a therapeutic candidate based on the gut microbiota.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179114"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GDF11 regulates hypoxia-induced pulmonary endothelial cell pyroptosis through SOX2/NLRP3 axis","authors":"Sijia Li,&nbsp;Hena Pan,&nbsp;LiuPing Wei,&nbsp;XinMeng Guo,&nbsp;Mingyu Yang,&nbsp;Jinhong Jia,&nbsp;Ying Zhao,&nbsp;Jianan Zhang,&nbsp;Xiaodong Zheng,&nbsp;Yajuan Ran,&nbsp;Xiufeng Yu","doi":"10.1016/j.ejphar.2026.179112","DOIUrl":"10.1016/j.ejphar.2026.179112","url":null,"abstract":"<div><h3>Background and objective</h3><div>Pulmonary arterial hypertension (PAH) is characterized by progressive pulmonary vascular remodeling, which is driven in part by endothelial dysfunction. Growth differentiation factor 11 (GDF11) has emerged as an important regulator of vascular homeostasis; however, its role in pulmonary artery endothelial cell (PAEC) pyroptosis remains unclear. This study aimed to define the contribution of GDF11 to hypoxia-induced PAH and its mechanistic association with inflammasome activation.</div></div><div><h3>Methods</h3><div>Endothelial-specific Gdf11 knockout mice were exposed to chronic hypoxia to evaluate hemodynamics, right ventricular hypertrophy, pulmonary vascular remodeling, and endothelial pyroptosis. In vitro, PAECs were subjected to GDF11 knockdown or adenoviral-mediated overexpression. Pyroptosis and downstream signaling were assessed by Western blotting, Annexin V/propidium iodide staining, lactate dehydrogenase release assay, Hoechst/propidium iodide imaging, immunofluorescence, and chromatin immunoprecipitation.</div></div><div><h3>Results</h3><div>GDF11 expression was increased in hypoxic lung tissues and PAECs. Endothelial-specific deletion of Gdf11 significantly reduced right ventricular systolic pressure, right ventricular hypertrophy, and pulmonary vascular remodeling, and suppressed hypoxia-induced PAEC pyroptosis. In vitro, GDF11 knockdown attenuated hypoxia-induced pyroptosis, whereas GDF11 overexpression exacerbated this response. Mechanistically, SOX2 was identified as a downstream transcriptional effector of GDF11 and was found to directly bind to the Nlrp3 promoter, thereby promoting inflammasome activation and pyroptosis.</div></div><div><h3>Conclusion</h3><div>These findings identify a previously unrecognized GDF11–SOX2–NLRP3 axis that promotes pulmonary endothelial pyroptosis and accelerates PAH progression. Targeting this pathway may provide new opportunities for biomarker development and therapeutic intervention in PAH.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179112"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GSK484 attenuates placental endothelial injury and improves gestation outcome in rats with preeclampsia by inhibiting PAD4-mediated neutrophil extracellular traps formation","authors":"Yuan-Yuan Li,&nbsp;Zhao-Yu Zhang,&nbsp;Jie Wang,&nbsp;De-Ping Wang,&nbsp;Wen-Fang Zhao,&nbsp;Hui-Jing Ma,&nbsp;Meng-Meng Lin,&nbsp;Ji-Min Cao,&nbsp;Ji-Bin Han","doi":"10.1016/j.ejphar.2026.179123","DOIUrl":"10.1016/j.ejphar.2026.179123","url":null,"abstract":"<div><div>Preeclampsia (PE) is a serious pregnancy disorder, but its pathogenesis has not been well elucidated and has no effective pharmacological therapy. Here we investigated the potential protective effect of GSK484, a selective inhibitor of peptidyl arginine deiminase 4 (PAD4), on PE in rats and the underlying mechanisms. PE was induced in pregnant rats by intravenous injection of low-dose lipopolysaccharides (LPS), and the general manifestations of PE were examined. The effects of GSK484 on placental expressions of PAD4 and vascular endothelial growth factor A (VEGFA), formation of neutrophil extracellular traps (NETs), placental neutrophil infiltration, and endothelial and microvasculature injury were measured using serial technologies including histology, ELISA, RT-qPCR, western blotting, immunofluorescent and immunohistochemical staining. Results show that LPS-treated pregnant rats exhibited PE-like symptoms and molecular pathologies, including late-onset hypertension, proteinuria, placental microvasculature and kidney injuries, growth restriction of the offspring, elevations of placental and circulatory PAD4, and formation of NETs which were composed of double-stranded DNA (dsDNA), myeloperoxidase (MPO) and citrullinated histone 3 (Cit H3) released from activated neutrophils. Administration of GSK484 (a PAD4 inhibitor) (2 mg/kg, <em>i. p.</em>) to pregnant rats reduced circulatory soluble fms-like tyrosine kinase 1 (sFlt-1), placental PAD4 expression and NETs formation, increased placental VEGFA expression and microvessel density (MVD), decreased blood pressure and urine proteins, and improved maternal body weight gain and offspring growth restriction. We conclude that GSK484 exerts a protective effect on rat PE mainly via inhibiting PAD4-mediated placental NETs formation, and ultimately improves maternal placental microvascular injury and benefits the pregnancy outcomes including mother and offspring. The study suggests that GSK484 may have the potential to be an effective drug in the treatment of PE.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179123"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural product clitorin reduces myocardial damage following acute myocardial infarction by mediating NOX4/Nrf2 redox balance","authors":"Xin Pan,&nbsp;Yonghao Yang,&nbsp;Chen Liu,&nbsp;Lei Xu,&nbsp;Junjun Yu,&nbsp;Sumin Ge,&nbsp;Wenxiu Wang,&nbsp;Cihan Wang,&nbsp;Wenping Wei,&nbsp;Sihua Wu,&nbsp;Kaizheng Gong","doi":"10.1016/j.ejphar.2026.179127","DOIUrl":"10.1016/j.ejphar.2026.179127","url":null,"abstract":"<div><h3>Purpose</h3><div>Acute myocardial infarction (AMI) is a severe cardiovascular disease to which excessive oxidative stress is a pivotal contributor. Clitorin (CL), a natural flavonoid from plants and fruits, has demonstrated antioxidant potential; however, its role and mechanism in AMI remain unclear. This study aimed to elucidate the protective effects and mechanisms of CL in AMI.</div></div><div><h3>Methods</h3><div>Forty-five male C57BL/6J mice were used to establish an AMI model by left anterior descending coronary artery ligation, followed by injection of 0.625, 1.25, or 2.5 mg/kg of CL. In vitro, oxygen-glucose deprivation (OGD) was induced in neonatal mouse cardiomyocytes (NMCMs), followed by administration of 10, 20, or 40 μM of CL. The therapeutic effects were assessed using triphenyltetrazolium chloride (TTC) staining, TUNEL staining, reactive oxygen species (ROS) staining, and flow cytometry. RNA sequencing, network pharmacology, SPR, CETSA, molecular docking, and Western blot were used for mechanistic studies.</div></div><div><h3>Results</h3><div>In vivo, CL exerted cardioprotective effects by reducing myocardial infarct size, decreasing apoptosis, and improving cardiac function. In vitro, CL mitigated OGD-induced ROS production in NMCMs, reduced apoptosis, and protected mitochondrial function. Mechanistically, CL protected against AMI by directly binding to NOX4 and regulating the NOX4/Nrf2 axis. By inhibiting NOX4, promoting Nrf2 upregulation and nuclear translocation, and alleviating mitochondrial damage and ferroptosis, CL exerted antioxidant effects and improved AMI-induced myocardial injury.</div></div><div><h3>Conclusion</h3><div>This study is the first to elucidate the cardioprotective role of CL in AMI by regulation of the NOX4/Nrf2 pathway. These findings deepen our understanding of CL in AMI.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179127"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A functional coupling of TRPA1 and TMEM16A channels regulates endothelium-dependent hyperpolarization-mediated vasorelaxation of mesenteric resistance arteries in healthy and septic mice","authors":"Yanan Zhang,&nbsp;Shaoya Rong,&nbsp;Shude Pang,&nbsp;Xiujun Fu,&nbsp;Yunxian Wang,&nbsp;Xuelu Ding,&nbsp;Shuai Liang,&nbsp;Ruihong Guo,&nbsp;Hui Dong","doi":"10.1016/j.ejphar.2026.179137","DOIUrl":"10.1016/j.ejphar.2026.179137","url":null,"abstract":"<div><div>Vascular endothelial dysfunction drives sepsis progression and multi-organ failure. Although TRPA1 and TMEM16A are expressed in the vasculature, their roles in arteriolar vasorelaxation remain unclear. The vasorelaxant effects of TRPA1 and TMEM16A on the second-order branch of mesenteric resistance arteries were investigated in healthy and septic mice using a Mulvany-style wire myograph. Fluorescent Ca²⁺ assays were employed to assess cytosolic Ca²⁺ ([Ca²⁺]_i) in vascular endothelial cells (VECs). A mouse sepsis model was constructed through the method of cecal ligation and puncture (CLP). Both TRPA1 and TMEM16A activation induced endothelium-dependent hyperpolarization (EDH)-mediated relaxation via functional coupling: TRPA1 triggered Ca²⁺ influx and Ca²⁺-induced Ca²⁺ release, amplifying TMEM16A activity. In sepsis, while ACh/EDH responses were impaired, TRPA1/TMEM16A-mediated relaxation remained intact. Channel activation improved septic mouse survival and restored ACh responses, with plasma and assay agonist concentrations in comparable ranges. This study not only elucidates the protective role of endothelial TRPA1 and TMEM16A channels against sepsis-induced vascular inflammation but also provides potential new targets for sepsis therapy.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179137"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intravenous immunoglobulin-resistant Kawasaki disease: diagnosis, mechanisms, and clinical management","authors":"Shuhui Wang,&nbsp;Yidan Zhang,&nbsp;Zhiyuan Liu,&nbsp;Miao Hou,&nbsp;Xuan Li,&nbsp;Yunjia Tang,&nbsp;Ye Chen,&nbsp;Ye Wang,&nbsp;Jiajia Tan,&nbsp;Panpan Liu,&nbsp;Mingyang Zhang,&nbsp;Yinghao Wang,&nbsp;Jing Li,&nbsp;Haitao Lv","doi":"10.1016/j.ejphar.2026.179135","DOIUrl":"10.1016/j.ejphar.2026.179135","url":null,"abstract":"<div><div>Intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD), also referred to as IVIG-refractory KD or refractory KD, is characterized by a high incidence of cardiovascular complications, particularly coronary artery lesions, and may result in severe outcomes that endanger the lives of affected children. Therefore, early identification, accurate diagnosis, and timely interventions are of paramount importance. In recent years, advances in epidemiological investigations, mechanistic studies, the establishment of high-risk predictive models, and pharmaceutical developments have created new opportunities for the early prediction and management of IVIG-resistant KD. This review summarizes the current research progress on IVIG-resistant KD, offering valuable perspectives for the prevention and clinical management of this condition.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179135"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Abca7-related microglial responses in linking type 2 diabetes mellitus to Alzheimer's disease progression: Evidence from single-cell transcriptomic analysis and experimental validation in animal and cell models","authors":"Ming Cheng,&nbsp;Xin Zheng,&nbsp;Ya-Dong Wei,&nbsp;Jin-Fang Ge","doi":"10.1016/j.ejphar.2026.179152","DOIUrl":"10.1016/j.ejphar.2026.179152","url":null,"abstract":"<div><div>Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) share overlapping pathological mechanisms characterized by neuroinflammation and metabolic dysfunction, yet the underlying mechanisms remain elusive. In this study, we aimed to investigate the potential involvement of <em>Abca7</em> in the microglial responses linking AD and T2DM. Single-cell RNA sequencing (scRNA-seq) data from the hippocampi of db/db and db/m mice were analyzed to characterize cellular heterogeneity. To validate the bioinformatic findings, an AD mouse model was established by a single intracerebroventricular injection of Aβ1-42. Behavioral performances were observed, and the protein expression of Abca7 and typical neuropathological features of AD were detected. In parallel, <em>in vitro</em> studies were conducted using BV2 microglial cells exposed to Aβ1-42 following <em>Abca7</em> knockdown. The scRNA-seq analysis revealed significant alterations in endothelial cells, microglia, and oligodendrocytes in db/db mice. Microglia emerged as central regulators of neuroinflammatory responses, with <em>Abca7</em> identified as a hub gene linked to both T2DM and AD pathology. Consistently, the expression of <em>Abca7</em> in the hippocampus of AD mice was markedly elevated and positively correlated with the cognitive impairments and Aβ/Tau pathology. Moreover, the knockdown of <em>Abca7</em> could protect BV2 cells against Aβ-induced injuries and hyperactivation which could be partly ascribed to the suppression of NF-κB signaling and oxidative stress. Overall, these results suggest <em>Abca7</em> may play a linking role in the microglial response between T2DM and AD, which is partly supported by <em>in vivo</em> and <em>in vitro</em> results of its effect on the hyperactivation of microglia in AD-like pathologies.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"1030 ","pages":"Article 179152"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Targeting the PTCHD1-hippo axis by rhPTH(1-34) restores contact inhibition and suppresses hyperproliferation in psoriatic keratinocytes\" [European J. Pharmacol. 1016 (2026) 178579].","authors":"Jing Guo, Wenqi Zhao, Liwei Feng, Xiaolin Bu","doi":"10.1016/j.ejphar.2026.179080","DOIUrl":"10.1016/j.ejphar.2026.179080","url":null,"abstract":"","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"179080"},"PeriodicalIF":5.7,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}