Inflammopharmacology最新文献

{"title":"Dexketoprofen enhances NLRP3 activation via ATPase activity after canonical stimuli.","authors":"Daniel Boy-Ruiz, Juan Miguel Suarez-Rivero, Inés Muela-Zarzuela, Mario D Cordero","doi":"10.1007/s10787-025-01928-2","DOIUrl":"https://doi.org/10.1007/s10787-025-01928-2","url":null,"abstract":"<p><p>Inflammasomes are crucial elements of the innate immune system, responsible for triggering inflammation through the activation of caspase-1. Among them, the NLRP3 inflammasome plays a central role in various inflammatory and immune-related disorders. Dexketoprofen (DXK) is a widely used nonsteroidal anti-inflammatory drug (NSAID), although it has not been tested for its effects on the NLRP3 inflammasome pathway. In this study, we explored the influence of DXK on NLRP3 activation and its associated inflammatory responses in human macrophages. Our results showed that even at low concentrations, DXK enhances the release of IL-1β and promotes cell death upon stimulation with LPS and ATP, nigericin and LPS and nigericin, indicating it increases inflammasome activation. Docking and ATPase assays revealed that DXK binds to the NLRP3 NATCH domain, facilitating ATP hydrolysis and NLRP3 activation. Furthermore, treatment with DXK in combination with nigericin further increased IL-1β secretion, while the NLRP3 inhibitor MCC950 reduced the effects of DXK. These findings suggest that DXK amplifies inflammation in macrophages via NLRP3 activation, emphasizing the importance of caution in prolonged use, especially in autoinflammatory diseases where inflammasomes play a significant role.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130534","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":"Limonene alleviated ulcerative colitis via anti-inflammation, anti-oxidation and regulating intestinal microenvironment in vivo and in vitro.","authors":"Wenxiu Xu, Hongbo Wang, Zhenyu Sun, Hui Zhang, Zhijun Zhang, Xiangrong Sun, Jiayu Gu, Yanling Gong","doi":"10.1007/s10787-025-01974-w","DOIUrl":"https://doi.org/10.1007/s10787-025-01974-w","url":null,"abstract":"<p><p>Limonene, a monoterpene naturally abundant in various Citrus fruits, is widely used as a fragrance component and dietary supplement. Ulcerative colitis (UC), a representative inflammatory bowel disease, is characterized by an arising incidence and considerable impact on human health. Although several reports have demonstrated the beneficial effects of limonene on UC, detailed mechanisms remain incompletely understood. In this study, we employed a dextran sulfate sodium (DSS)-induced UC murine model and a lipopolysaccharide (LPS)-stimulated Caco-2 cell model to explore the mechanisms of limonene on UC. The results revealed that limonene significantly decreased disease activity index (DAI) score and alleviated pathological damage in UC mice, exhibiting therapeutic potential for UC. Limonene significantly inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) while increased superoxide dismutase (SOD) in both DSS-induced UC mice and LPS-induced Caco-2 cells. Furthermore, limonene significantly increased expressions of Zonula occludens-1 (ZO-1), occludin, and claudin-1, thereby enhancing intestinal barrier integrity. Limonene mitigated UC-associated dysbiosis by shifting the gut microbial composition toward that of healthy controls. Specifically, it modulated the microbiota at the phylum, family, genus and species levels, increasing the abundance of anti-inflammatory bacteria while decreasing inflammatory related taxa. Collectively, our in vivo and in vitro results demonstrate that limonene alleviates UC involving in anti-inflammation, anti-oxidation, restoration of intestinal barrier integrity and regulation of the gut microbiota. Future studies are warranted to explore whether gut microbial metabolites contribute to the protective effects of limonene in UC.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124710","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":"Targeting mGluR7 in Parkinson's disease: a novel approach to neuroprotection and synaptic therapies.","authors":"Gursimran Singh, Khadga Raj Aran","doi":"10.1007/s10787-025-01921-9","DOIUrl":"https://doi.org/10.1007/s10787-025-01921-9","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by dopaminergic neuronal loss in the substantia nigra pars compacta (SNPC) and complex motor and non-motor symptoms. Emerging evidence underscores excitotoxic glutamatergic overactivity as a key pathological driver of neurodegeneration, in addition to neuronal loss caused by dopamine depletion. Among the metabotropic glutamate receptors (mGluRs), mGluR7, a presynaptically located G protein-coupled receptor, has gained significant attention due to its unique low-affinity and high-threshold profile, which allows for selective modulation during synaptic hyperactivity while preserving physiological neurotransmission. mGluR7 is a glutamate sensor and inhibitor of glutamate release, modulating excitotoxicity, neuroinflammation, synaptic plasticity, and mitochondrial integrity, which are key features of PD neuropathology. It is highly expressed in basal ganglia loops and glial cells, providing dual-regulatory functionality in neuronal and immune microenvironments. Positive allosteric modulators of mGluR7 represent a potentially exciting group of compounds to increase receptor activity specifically during hyperglutamatergic conditions. In addition to monotherapy, mGluR7 modulators have significant value in the context of combined or stratified therapies, since they enhance dopaminergic therapy and restore synaptic dysfunction. Moreover, current developments in CRISPR-Cas9, RNAi, viral vectors, and nanomedicine offer new arenas to regulate mGluR7 expression and activity with precision. Translating preclinical success into clinical therapies is now feasible with advances in mGluR7-specific PET tracers, biomarkers, and patient profiling. Together, these findings position mGluR7 as a highly promising therapeutic target. This review critically explores the molecular structure, signaling mechanisms, and CNS distribution of mGluR7 by highlighting its role in modulating excitotoxicity, synaptic dysfunction, neuroinflammation, and mitochondrial stress in PD. It also examines the pharmacological development of mGluR7-targeted agents, their preclinical effects on motor and non-motor symptoms, and their potential in combination therapies. Emerging strategies such as CRISPR, RNAi, nanomedicine, and the development of mGluR7-specific biomarkers and imaging tools are also explored to support precision medicine in PD.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124015","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 hydroalcoholic extract of the leaves of red mombin (Spondias purpurea L.) is more effective in accelerating ulcer healing than preventing them in rodents.","authors":"Ruan Kaio Silva Nunes, Bruna Longo, Caio Henrique Willrich, Levy Mota da Silva, Luísa Santiago, Thiago Farias de Queiroz Silva, Lucas Matheus Lessa de Olinda, Layla Francielle Pereira, Heloisa Immianovsky Eisendecker, José Roberto Santin, Larissa Benvenutti, Luiza Felipim Corsi, Bianca Priscila Miranda, Hydima Julião Cóta, Larissa Venzon, Tauani Caroline Santos França, Max Vidal-Gutiérrez, Zuleide Maria Ignacio, Walter Antônio Roman-Junior, Luísa Mota da Silva","doi":"10.1007/s10787-025-01915-7","DOIUrl":"https://doi.org/10.1007/s10787-025-01915-7","url":null,"abstract":"<p><p>This study evaluated the anti-ulcer effects of the hydroalcoholic extract from the leaves of Spondias purpurea L. (SPHE). The gastroprotection was assessed using acidified ethanol-induced gastric ulcer in mice given orally with the vehicle, carbenoxolone (200 mg/kg), or SPHE (10-1.000 mg/kg). The extract's healing activity was evaluated using acetic acid-induced ulcers in rats treated with vehicle, omeprazole (20 mg/kg), or SPHE (3-300 mg/kg). Histological and biochemical analyses were done in ulcerated tissue from both models. SPHE antisecretory action was tested in pylorus-ligated rats. The in vitro antioxidant potential was assessed using the DPPH test; its cytotoxicity and proliferative effects were measured in L929 cells. Mass spectrometry analysis was used to determine the extract's chemical profile and the quantification of phenolic compounds in the extract was performed in LCMS. SPHE induced gastroprotection at a dose of 1.000 mg/kg, and this effect was lost in mice treated with NEM, indomethacin, or yohimbine but not L-NAME. SPHE improves the healing of acetic acid-induced ulcers by 69.5% and 83.7% at 10 and 30 mg/kg, respectively. The microscopic examination confirms the healing effect of SPHE. SPHE enhanced PAS-stained mucins, SOD, and GST activities while decreasing MPO activity, and MDA levels in ulcerated mucosa, and scavenged DPPH radicals but did not change the gastric acid secretion. SPHE showed no cytotoxicity and favored fibroblast proliferation. The presence of hibiscus acid, hydroxy citric acid, hibiscus acid glycoside, ellagic acid, and the flavonoids quercetin and rutin were confirmed and quercetin, caffeic acid, p-coumaric acid, gallic acid, and epigallocatechin were quantified. Therefore, SPHE accumulated chemicals with higher gastric healing potential mediated by gastric protective features, specifically antioxidant resources, mucus barrier, and cell proliferation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130727","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":"Potentiation of analgesic activity following the complexation of Algrizea minor Sobral, Faria & Proença (Myrteae, Myrtaceae) leaf essential oil with β-cyclodextrin.","authors":"Paulo Henrique Eloi Fernandes, Bruno Oliveira de Veras, Paulo Henrique Andrade do Nascimento Silva, Júlio César Ribeiro de Oliveira Farias de Aguiar, Daniela Maria do Amaral Ferraz Navarro, Maria Tereza Dos Santos Correia, Márcia Vanusa da Silva","doi":"10.1007/s10787-025-01979-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01979-5","url":null,"abstract":"<p><p>Pain is a fundamental biological process; however, its acute manifestation may result in dysregulation and tissue injury. The Myrtaceae family is well known for its diverse pharmacological activities, and Algrizea minor, a species native to Brazil, has traditionally been used for the management of inflammation and pain. The present study investigated the antinociceptive properties of essential oil Algrizea minor (EOAm) and examined whether its complexation with β-cyclodextrin (β-CD) could enhance its pharmacological efficacy. EOAm was obtained by hydrodistillation, yielding 0.57% (w/w), with β-pinene (66.99%) identified as the major constituent. Antinociceptive activity was evaluated using murine models, including the acetic acid-induced writhing and formalin tests. Free EOAm significantly reduced nociceptive behavior in a dose-dependent manner, producing up to 89% inhibition in the acetic acid model. Remarkably, complexation with β-CD further potentiated the analgesic effect, achieving complete inhibition of nociception at the highest dose tested (200 mg/kg). In the formalin assay, both EOAm and its β-CD complex displayed significant efficacy during the neurogenic and inflammatory phases. Partial reversal of the analgesic effect by naloxone indicates the involvement of the opioid system in the underlying mechanism. Overall, these findings demonstrate that EOAm possesses strong antinociceptive activity, which is further enhanced through β-cyclodextrin complexation. This approach not only improves efficacy but also may increase the stability and bioavailability of the essential oil, highlighting the EOAm/β-CD complex as a promising candidate for the development of novel analgesic therapies.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124661","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":"Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.","authors":"Zeynab Marzhoseyni, Foroogh Neamati, Mansoor Khaledi, Mohammad Hossein Haddadi, Aydin Sadeghi, Mina Yekani, Mohammad Yousef Memar","doi":"10.1007/s10787-025-01957-x","DOIUrl":"https://doi.org/10.1007/s10787-025-01957-x","url":null,"abstract":"<p><p>Gastric cancer (GC) remains a significant global health burden with Helicobacter pylori (H. pylori) infection considered a primary risk factor. However, the precise molecular mechanisms of this relationship are still being elucidated. Recent studies have revealed that long non-coding RNAs (lncRNAs) play a crucial role in regulating gene expression, significantly impacting various biological processes, including carcinogenesis. LncRNAs are non-protein-coding transcripts that are over 200 nucleotides long. It has been reported that lncRNAs play a dual role, in promoting or inhibiting cancer progression through intricate molecular pathways in H. pylori-associated GC. The aim of this study was to provide an overview of the role of lncRNAs in the pathogenesis of GC induced by H. pylori. Upregulated lncRNAs such as H19, GClnc1, LINC00152, and PVT1 in H. pylori-infected patients contribute to tumorigenesis by enhancing cell proliferation, migration, invasion, and inflammation. This is often achieved through interactions with oncogenic pathways, stabilization of pro-tumor proteins, or acting as sponges for tumor-suppressive microRNAs. The mechanisms of lncRNA action are diverse, encompassing epigenetic, transcriptional, and post-transcriptional regulation, as well as influencing protein interactions and key signaling pathways, such as Wnt/β-catenin, PI3K/AKT, and NF-κB. Furthermore, lncRNAs are implicated in DNA damage and genomic instability induced by H. pylori, as well as in creating the tumor microenvironment by regulating angiogenesis and immune evasion. This multifaceted involvement positions lncRNAs as promising diagnostic, prognostic, and therapeutic markers for H. pylori-associated GC, warranting further investigation for novel clinical interventions.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075200","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 impact of alpha-lipoic acid treatment on various mediators of inflammatory and immune responses in a murine arthritis model.","authors":"Mohamad M Aboelenin, Mohamed Hefnawy, Talha Bin Emran, Heba I Shafey, Khairy M A Zoheir","doi":"10.1007/s10787-025-01941-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01941-5","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by inflammation in the synovial lining of joints, leading to pain, stiffness, and significant functional limitations. Current treatments focus on managing symptoms and slowing disease progression, but they often have side effects and may not be effective for all patients. This study investigated the effects of alpha-lipoic acid (ALA) on immune response and inflammation in mouse model of arthritis. Adjuvant-induced arthritis (AIA) was established in mice, and ALA was administered to mice at a dose of 75 mg/kg via oral gavage twice daily for 7 consecutive days. ALA administration significantly reduced arthritis severity, as evidenced by decreased paw oedema and arthritis score. ALA treatment led to a significant reduction in plasma levels of IL-17A, TNF-α, and MMP-3, key biomarkers of arthritis disease activity. ALA decreased the number of circulating Th17 and NF-κB p65⁺ CD4⁺ T lymphocytes, suggesting its potential to modulate the immune response. ALA downregulated the expression of pro-inflammatory genes (IL17F, TNF) and upregulated the expression of the anti-inflammatory cytokine IL10 gene in the joint tissues. In the joint tissue, ALA modulated the expression of NFKB1, STAT3, GATA3, TBX21, and RORC, all of which are key transcription factors associated with arthritis pathogenesis. Molecular docking results suggest potential binding interactions between ALA and key molecules like GATA-3 and TNF-α, as a potential mechanism for its anti-inflammatory properties. These findings support ALA's potential as a promising therapeutic agent for RA in human patients, as it appears to modulate inflammation, immune responses, and key molecular pathways involved in disease pathogenesis.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075251","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":"Natural products and nutraceuticals in the management of chronic inflammatory diseases: efficacy, mechanisms, and comparative insights.","authors":"Polu Picheswara Rao","doi":"10.1007/s10787-025-01954-0","DOIUrl":"https://doi.org/10.1007/s10787-025-01954-0","url":null,"abstract":"<p><p>Chronic inflammatory diseases represent a significant global health burden, driving increased exploration of natural products and nutraceuticals as complementary or alternative therapeutic options. This review provides a comprehensive evaluation of the molecular and cellular mechanisms by which natural compounds modulate inflammatory pathways, focusing on their antioxidant, immunomodulatory, and anti-inflammatory effects distinct from conventional nonsteroidal anti-inflammatory drugs (NSAIDs). Drawing on evidence from recent clinical trials and preclinical animal studies, we examine their therapeutic potential across diverse inflammatory conditions including gastrointestinal disorders, rheumatic diseases, neuroinflammation, and inflammation-associated muscle dysfunction related to aging and injury. The article critically compares the efficacy and safety profiles of natural agents with established pharmacological therapies, emphasizing advantages and limitations supported by current data. Furthermore, regulatory considerations, challenges in standardization, and quality control issues surrounding natural products are discussed, alongside their integration into personalized treatment regimens. By highlighting gaps in knowledge and emerging avenues for research, such as discovery of novel bioactive compounds and improved clinical trial designs, this review aims to guide future investigations and clinical application. Overall, the synthesis offers valuable insights for researchers, clinicians, and policymakers seeking innovative and safe anti-inflammatory strategies grounded in natural product research.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075262","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":"Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.","authors":"Ali M Elgindy, Ahmed M Atwa, El-Sayed E El-Awady, Norhan M El-Sayed, Naglaa F El-Orabi","doi":"10.1007/s10787-025-01889-6","DOIUrl":"https://doi.org/10.1007/s10787-025-01889-6","url":null,"abstract":"<p><p>Renin-Angiotensin System has been implicated in neurodegenerative diseases such as Huntington's (HD). It is made up of two axes: one is the Angiotensin II Type 1 receptor (AT1R) or Angiotensin II Type 2 receptor (AT2R), while the other is angiotensin-(1-7) [Ang-(1-7)], and Mas receptor; the latter has reported developing a neuroprotective effect; oppositely, AT1R activation has been linked to neurodegenerative diseases. This study aims to elucidate the potential neuroprotective effect of Candesartan (Cand) an AT1R blocker in mitigating neuronal degeneration caused by 3-Nitropropionic acid (3NP) induced HD by revealing the prospective role of Ang II/AT2R/Ang-(1-7)/Mas receptor, CREB/BDNF/PGC1-α besides JNK/c-Jun trajectories, as well as the anti-apoptotic survivin. HD was induced by 3NP (10 mg/kg) for 14 days. Rats received Candesartan (2.5 or 5 mg/kg) for 14 days, after which brain and striatum were isolated for the histopathological, immunohistochemical, and biochemical analysis. Cand displayed significant improvement in the rats' behavioral tests, enhancing their memory, motor, and cognitive functions induced by 3NP, which was confirmed by the striatal histopathological and immunohistochemical examination of the GFAP. In addition, Cand activated the Ang II/AT2R/Ang-(1-7)/Mas receptor axis. Moreover, Cand stimulated the production of striatal neurotrophic proteins CREB/BDNF/PGC1-α which in turn decreased the levels of inflammatory mediators NF-κB and IL-1β, accompanied by an increase in the antioxidants NQO1 and HO-1 levels. Similarly, Cand led to the inhibition of the JNK/c-Jun with activation of survivin. In conclusion, Candesartan has mitigated the striatal degeneration and mitochondrial dysfunction induced by 3NP through various mechanistic pathways.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069331","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":"Pharmacological interventions targeting β-adrenoceptors in colorectal cancer: an evolving paradigm.","authors":"Aya Ghosn, Khalil Bassam, Mohammad Al Zein, Suzanne A Nasser, Gianfranco Pintus, Ali H Eid","doi":"10.1007/s10787-025-01925-5","DOIUrl":"https://doi.org/10.1007/s10787-025-01925-5","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a significant global health challenge, ranking as the third most common cancer and the second leading cause of cancer-related deaths worldwide. Its development is influenced by several risk factors, including smoking, diets rich in red meat, and the effects of stress-related hormones such as epinephrine and norepinephrine. These hormones act through β-adrenergic receptors (β-ARs), which are present on CRC cells and are associated with cancer-promoting processes such as increased cell growth, invasion, blood vessel formation, and accelerated disease progression. Notably, β-ARs blockers have shown potential in slowing CRC progression, pointing to a promising therapeutic strategy. This review explores the main signaling pathways through which β-ARs contribute to cancer development and how various risk factors may influence these mechanisms. We also provide an overview of current preclinical and clinical studies on β-AR blockers in CRC, identify existing gaps in knowledge, and propose directions for future research to optimize therapeutic outcomes.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145064387","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}