Pharmacology最新文献

{"title":"Heterogeneity and Regulatory Mechanisms of ALK-Mutant and Wild-Type Epithelial Cells in Non-Small-Cell Lung Cancer: Single-Cell Transcriptomics and Chromatin Accessibility.","authors":"Yafu Zhou, Manni Yi, Jianhua Yan, Huiguo Chen, Jingsong Yang","doi":"10.1159/000550967","DOIUrl":"10.1159/000550967","url":null,"abstract":"<p><strong>Introduction: </strong>Anaplastic lymphoma kinase (ALK) mutations are key oncogenic drivers in non-small-cell lung cancer (NSCLC). Although ALK tyrosine kinase inhibitors (TKIs) elicit high initial response rates, relapse due to acquired resistance is common. Conventional approaches fail to resolve tumor heterogeneity and epigenetic control, necessitating multi-omic integration to dissect molecular differences between ALK-mutant and wild-type (WT) tumors.</p><p><strong>Methods: </strong>Single-cell RNA sequencing (scRNA-seq) and matched chromatin accessibility (scATAC-seq) data of 5 WT and 4 ALK-mutant NSCLC samples from GEO (GSE274934) were integrated. \"Seurat\" and \"Harmony\" packages in R were used for data preprocessing and batch correction. \"Monocle\" package reconstructed epithelial differentiation trajectories. \"CellChat\" package delineated cell-cell communication. \"Signac\" package integrated multiple omics data and analyzed the differentially accessible chromatin regions. Motif enrichment based on the JASPAR database identified key transcription factors. The role of CEACAM6 in the malignant progression of ALK-mutant-mutant NSCLC was assessed by qRT-PCR, CCK-8, colony formation, and wound-healing assays.</p><p><strong>Results: </strong>ALK-mutant epithelial cells exhibit disrupted differentiation trajectories, characterized by loss of SPINK1 expression and pan-expression of MARCKSL1. ALK-mutant cells relied on CEACAM5/6 signaling for communication; WT cells primarily engaged in multidirectional MIF interactions. ALK-mutant cells showed increased global chromatin accessibility. Motif analysis revealed enrichment of polycomb repressive complex (PRC) pathway components and EGR1 binding sites (survival/drug resistance-associated) in ALK-mutant cells, whereas WT cells specifically enriched KLF5, ZNF148, and GLIS3 motifs. In vitro, CEACAM6 expression was significantly upregulated in ALK-mutant compared to WT cells. CEACAM6 knockdown significantly inhibited cell proliferation and migration, and reduced p-AKT and EGR1 protein levels, indicating that CEACAM6 promotes malignant progression of ALK-mutant NSCLC through the AKT-EGR1 signaling axis.</p><p><strong>Conclusion: </strong>ALK mutations drive tumor stemness and drug resistance by blocking epithelial cell differentiation, activating CEACAM6-mediated signaling, enhancing chromatin accessibility, and remodeling the EGR1/PRC regulatory network. Targeting CEACAM6 and its downstream effector EGR1 may represent an effective strategy to overcome ALK-TKI resistance.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"153-173"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of the Mevalonate Pathway Targets Neuroblastoma Stem Cells.","authors":"Michelle V Green, Jessie L Reed, Cameron D Zielinski, Jeffrey D Neighbors","doi":"10.1159/000549949","DOIUrl":"10.1159/000549949","url":null,"abstract":"<p><strong>Introduction: </strong>High-risk neuroblastoma is a difficult-to-treat cancer with high rates of recurrence and treatment resistance, likely driven by a population of cancer stem cells. Multiple previous studies have suggested that the use of mevalonate pathway inhibitors, such as statins and bisphosphonates, may have anticancer activity against high-risk tumors.</p><p><strong>Methods: </strong>We aimed to observe the use of mevalonate pathway inhibitors against the cancer stem cell population of high-risk neuroblastoma cell lines SH-SY5Y, SK-N-AS, and SK-N-BE(2)-C using spheroid-based assays.</p><p><strong>Results: </strong>We observed significant reductions in spheroid formation capability, stem cell frequency, and stemness properties of these neuroblastoma cancer stem cells with fluvastatin and zoledronate treatment.</p><p><strong>Conclusion: </strong>Treatment with mevalonate pathway inhibitors leads to reduced neuroblastoma cancer stem cell function through reductions in protein geranylgeranylation.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"10-32"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Autophagy to Restore Intestinal Integrity in Sepsis: Resveratrol's NOX1/SIRT1-Mediated Protective Effect.","authors":"Wei Zhang, Jiang Yu, Zhongliang Shi, Yanna Jiao, Zhizhen Lai, Jiahua Chi, Jiayan Li, Jianbiao Meng","doi":"10.1159/000550966","DOIUrl":"10.1159/000550966","url":null,"abstract":"<p><strong>Introduction: </strong>A serious complication of sepsis that directly impacts patient outcomes is intestinal barrier disruption. Although the polyphenolic molecule resveratrol (RE) is well known for its anti-inflammatory and antioxidant properties, its specific role in targeting the NADPH oxidase 1 (NOX1)/sirtuin 1 (SIRT1) pathway to protect against sepsis-induced intestinal barrier failure remains unexplored. Therefore, this study aimed to comprehensively investigate this novel mechanism.</p><p><strong>Methods: </strong>The lipopolysaccharide (LPS)-treated Caco-2 cells and sepsis mouse models (cecal ligation and puncture) were utilized to assess the protective effects of RE. Quantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, histological analysis, immunohistochemistry, and Western blot were employed to examine inflammatory cytokine levels, autophagy markers, and intestinal barrier function. The roles of NOX1 and SIRT1 in RE-mediated protection were explored through NOX1 overexpression and related molecular analyses.</p><p><strong>Results: </strong>RE significantly improved survival rates in sepsis mice, reduced inflammatory cytokines, and restored intestinal barrier function. RE reversed the increase of NOX1 and the decrease of SIRT1 in sepsis. Histological analysis data showed that RE protected the intestinal structure, maintained the expressions of tight junction proteins, and alleviated intestinal damage. In LPS-treated Caco-2 cells, RE inhibited inflammation, promoted autophagy, and suppressed reactive oxygen species production. NOX1 overexpression partially offset the protective effects of RE.</p><p><strong>Conclusion: </strong>By modifying the NOX1/SIRT1 signaling pathway, RE protects against sepsis-induced intestinal barrier failure. These results underline that the NOX1/SIRT1 pathway is instrumental in autophagy and inflammation control and that RE may be a viable treatment approach for sepsis-related intestinal damage.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"114-134"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147318127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tocilizumab Biosimilars versus Reference Tocilizumab in Rheumatoid Arthritis: A Meta-Analysis of Pharmacokinetic Biosimilarity, Efficacy, Safety, and Immunogenicity.","authors":"Young Ho Lee, Gwan Gyu Song","doi":"10.1159/000552447","DOIUrl":"10.1159/000552447","url":null,"abstract":"<p><p><p>Introduction: The aim of the study was to systematically evaluate the efficacy, safety, immunogenicity, and pharmacokinetics (PK) of tocilizumab biosimilars compared to reference tocilizumab (r-TCZ) in patients with rheumatoid arthritis (RA) and healthy volunteers.</p><p><strong>Methods: </strong>We searched PubMed, Embase, and Cochrane CENTRAL for phase I and III randomized controlled trials (RCTs) comparing tocilizumab biosimilars vs. r-TCZ. Primary outcomes included change from baseline in DAS28-ESR, ACR20/50/70 response rates, adverse events (AEs), serious AEs (SAEs), anti-drug antibody (ADA) positivity, and PK parameters (AUC_0-inf, C_max, and AUC_0-last). Random-effects meta-analyses were performed using mean difference (MD), risk ratio (RR), and geometric mean ratio (GMR) with 95% or 90% confidence intervals (CIs). This systematic review and meta-analysis have been registered in PROSPERO (CRD420251270353).</p><p><strong>Results: </strong>Eight studies met the inclusion criteria, comprising 3 phase III RCTs (n = 1,696 RA patients) and 5 phase I RCTs (n = 1,363 healthy volunteers), for a total of 3,059 participants. In RA patients, biosimilars demonstrated equivalent efficacy to r-TCZ at week 24, with no significant differences in DAS28-ESR change (MD -0.06; 95% CI: -0.19 to 0.06; I2 = 0%) or ACR20 response rates (RR 1.03; 95% CI: 0.96-1.10; I2 = 0). Results for ACR50 and ACR70 were similarly balanced. Safety profiles were comparable (any AE: RR 1.01; 95% CI: 0.94-1.08), as was immunogenicity (ADA positivity: RR 1.28; 95% CI: 0.99-1.65). In healthy volunteers, PK biosimilarity was confirmed across intravenous and subcutaneous routes with pooled GMRs (90% CI) of 104.5% (101.2-107.9%) for AUC_0-inf, 101.4% (98.5-104.4%) for C_max, and 102.3% (97.8-106.9%) for AUC_0-last; all pooled CIs lay entirely within the 80-125% regulatory acceptance range (I2 ≤ 35).</p><p><strong>Conclusion: </strong>Tocilizumab biosimilars exhibit therapeutic similarity in RA patients and pharmacokinetic biosimilarity in healthy volunteers compared to r-TCZ, with comparable safety and immunogenicity, supporting their use as credible, cost-effective alternatives in clinical practice. </p>.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"205-218"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13341084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Statement.","authors":"","doi":"10.1159/000552108","DOIUrl":"10.1159/000552108","url":null,"abstract":"<p><p>The article \"Hypoxia-Treated Adipose Mesenchymal Stem Cells Derived Exosomes Enhance the Therapeutic Effects on Unilateral Ureteral Obstruction Mice\" [Pharmacology. 2025;110(3):165-177; https://doi.org/10.1159/000542609] by Chi Zhang, Longjun Cai, Meimei Ma, Xiaohui Xie, Junsheng Wang and Yuanyuan Zhang has been retracted by the Publisher and the Editor.After the publication of this article, it was identified that Figure S1c in this article, depicting confirmation of the capability of the AMSCs for adipogenic differentiation, had been previously published as Figure 1C by a different author group depicting the capability of primary mouse BMSCs to differentiate to adipocytes [1].When asked to comment on the above, the authors stated that the image in question was provided by the stem cell distributor and that they did not conduct the differentiation experiments depicted in Figure S1, which was not disclosed in the article. As the authors did not disclose the source of the experiments and images in the figure in question and did not independently characterise the cell population before the study was conducted, the Editor concluded that the concerns undermined the results of the article and, therefore, the article has been retracted.The authors agreed to this retraction.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"219-220"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148043556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimal pulse technology combined with tobramycin and dexamethasone eye ointment in the treatment of blepharokeratoconjunctivitis: an impact on ocular surface disease index.","authors":"Jing Yuan, Biyue Tu, Zhen Zhao, Yanxia Tong","doi":"10.1159/000548649","DOIUrl":"https://doi.org/10.1159/000548649","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to unveil the impact of optimal pulse technology (OPT) combined with tobramycin and dexamethasone eye ointment on the ocular surface disease index (OSDI) and related outcomes in patients with blepharokeratoconjunctivitis (BKC).</p><p><strong>Methods: </strong>Ninety-six BKC patients treated at our hospital from September 2022 to September 2023 were divided into a control group (n = 48) and an observation group (n = 48) by a random number table. Both groups received fluorometholone and sodium hyaluronate eye drops. The control group additionally applied tobramycin and dexamethasone eye ointment to the lid margin twice daily, while the observation group underwent OPT on this basis. The clinical efficacy and safety, OSDI, conjunctival hyperemia score, lid margin alteration score, meibomian gland yield secretory score (MGYSS), Demodex mite count, and tear break-up time (TBUT) were compared between the two groups before treatment and at 4 and 8 weeks post-treatment. Additionally, the National Eye Institute Visual Function Questionnaire-25 (NEIVFQ-25) scores were assessed before and after treatment.</p><p><strong>Results: </strong>The total effective rate in the observation group was 100.00% (48/48) at 8 weeks post-treatment, higher than 89.58% (43/48) in the control group (P < 0.05). The OSDI, conjunctival hyperemia score, lid margin alteration scores, MGYSS, and Demodex mite count all decreased in both groups at 4 and 8 weeks post-treatment compared to baseline, with greater improvements in the observation group(P < 0.05). TBUT and NEIVFQ-25 scores increased in both groups at 8 weeks post-treatment compared to baseline, with the observation group achieving better outcomes than the control group (P < 0.05).</p><p><strong>Conclusion: </strong>The addition of OPT to standard therapy for BKC is safe and provides superior short-term efficacy. It can alleviate lid margin inflammation, improve ocular surface symptoms, and enhance visual-related quality of life.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-17"},"PeriodicalIF":3.2,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145378417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drug-Drug Interactions in Hospitalized Urological Patients: A Retrospective Cohort Study.","authors":"Ivan R Milovanovic, Ana V Pejcic","doi":"10.1159/000540427","DOIUrl":"10.1159/000540427","url":null,"abstract":"<p><strong>Introduction: </strong>Exposure to potential drug-drug interactions (pDDIs) can be a notable source of avoidable drug-related harm that requires adequate management to prevent medical errors. We aimed to evaluate pDDIs and associated factors in hospitalized urological patients on admission, during hospitalization, and on discharge.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted at the Clinic of Urology of the University Clinical Centre Kragujevac, Serbia. To detect pDDIs, we used Lexicomp, which categorizes pDDIs as follows: X (avoid combination), D (consider therapy modification), C (monitor therapy), B (no action needed), and A (no known interaction). Multiple linear regression analysis was used to identify factors associated with the number of pDDIs.</p><p><strong>Results: </strong>More than half of the 220 included patients had at least one pDDI on admission and discharge (57.3% and 63.6%, respectively), whereas 95.0% had at least one pDDI during hospitalization. The total number and number of X, D, C, and B categories of pDDIs were the highest during hospitalization and the lowest on admission. Duration of hospitalization, arrhythmias, dementia, renal failure, cancer, surgery during hospitalization, number of prescribed drugs, and various pharmacological drug classes were risk factors for a higher number of pDDIs, while age, ischemic heart disease, hypertension, and development of infection during hospitalization were protective factors in at least one of the stages. The impact of renal colic depended on the stage and category of pDDI.</p><p><strong>Conclusion: </strong>More than half of the urological patients were exposed to at least one pDDIs at all stages. Medical professionals should regularly screen for pDDIs, particularly in patients with risk factors.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"15-25"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen Receptors and Platelet-Activating Acetylhydrolase Activity in the Pathogenesis of Systemic Lupus Erythematosus.","authors":"Akira Sato, Yuta Ogawa, Ayano Yabuki, Genta Sato, Hina Nemoto, Makoto Ohira, Akira Sato","doi":"10.1159/000543797","DOIUrl":"10.1159/000543797","url":null,"abstract":"<p><strong>Introduction: </strong>Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects various body systems, including the skin and facial features. Estrogen promotes lupus in human and mouse models of SLE. In this study, we conducted an in vivo study to investigate the relationship between two estrogen receptors (ER_α and ER_β) and platelet-activating factor acetylhydrolase (PAF-AH) on the symptoms of SLE.</p><p><strong>Methods: </strong>Skin and facial features, serum PAF-AH activity, tumor-necrosis factor-alpha (TNF-α), and anti-double stranded DNA (anti-dsDNA) antibody titer, all of which are central to the classification and pathogenesis of SLE, were measured in SLE model mice injected with various ER antagonists.</p><p><strong>Results: </strong>In SLE mice, the injection of an ER_β antagonist 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-α]pyrimidine-3-yl]-phenol induced the expression of facial erythema (especially around a cheek). The injection of an ER_α/β antagonist tamoxifen induced hair-loss on the head and the neck. The injection of an ER_α antagonist methylpiperidino pyrazole or tamoxifen increased PAF-AH activity and decreased TNF-α levels and anti-dsDNA antibody in mouse serum.</p><p><strong>Conclusions: </strong>The activation of ER_α and inactivation of ER_β can cause inflammatory and cutaneous symptoms of SLE, respectively, implying that ER_α antagonists and/or ER_β agonists can be useful for the prevention and treatment of SLE.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"254-260"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UCF101 Rescues against Diabetes-Evoked Cardiac Remodeling and Contractile Anomalies through AMP-Activated Protein Kinase-Mediated Induction of Mitophagy.","authors":"Zhiqiang Zhuang, Yuxi Zhu, Jun Tao, Yandong Liu, Jie Lin, Chunjie Yang, Chule Dong, Xing Qin, Qun Li, Russel J Reiter, Guizhen Wang, Zhaohui Pei, Jun Ren","doi":"10.1159/000541569","DOIUrl":"10.1159/000541569","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetes mellitus is known to provoke devastating anomalies in myocardial structure and function, while effective therapeutic regimen is still lacking. The selective protease inhibitor UCF101 (5-[5-(2-nitrophenyl) furfuryl iodine]-1,3-diphenyl-2-thiobarbituric acid) has been shown to fend off ischemic heart injury, although its impact on diabetic cardiomyopathy remains elusive.</p><p><strong>Methods: </strong>Our present work was conducted to examine the effect of UCF101 on experimental diabetes-evoked cardiac geometric and functional abnormalities as well as mechanisms involved. Adult mice were made diabetic using streptozotocin (STZ, 50 mg/kg, i.p., for 5 days) while receiving UCF101 (7.15 mg/kg, i.p.).</p><p><strong>Results: </strong>STZ evoked cardiac hypertrophy, interstitial fibrosis, mitochondrial ultrastructural damage, oxidative stress, dampened autophagy (LC3B, Beclin 1, elevated p62), mitophagy (FUNDC1 and Parkin with upregulated TOM20), increased left ventricular end systolic diameter, reduced fractional shortening, ejection fraction, cardiomyocyte shortening capacity, velocities of shortening/re-lengthening, and rise in intracellular Ca2+ in conjunction with elongated diastole and intracellular Ca2+ removal, the responses were overtly reconciled by UCF101 with little effects from UCF101 itself. Levels of cell injury markers Omi/HtrA2, TNFα, and stress signaling (JNK, ERK, p38) were overtly enhanced along with compromised phosphorylation of cellular fuel AMP-activated protein kinase (AMPK) (Thr172) and cell survival molecule GSK3β, as well as downregulated SERCA2a and elevated phospholamban, the effect was reversed by UCF101 (except for SERCA2a). AMPK knockout, pharmacological inhibition, the mitophagy inhibitor liensinine, and parkin knockout nullified UCF101-offered cardioprotection in diabetes. UCF101 reversed STZ-induced upregulation in the AMPK degrading enzymes PP2A and PP2C.</p><p><strong>Conclusion: </strong>These findings suggest that UCF101 rescues diabetes-mediated alterations in cardiac structure and function, likely through AMPK-mediated regulation of mitophagy.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"127-140"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese Medicine Formulas for the Treatment of Sepsis-Induced Acute Lung Injury: A Review.","authors":"Ling Sun, Hongya Gan, Qing Ye","doi":"10.1159/000547633","DOIUrl":"10.1159/000547633","url":null,"abstract":"<p><strong>Background: </strong>Sepsis, a severe infectious systemic syndrome with high morbidity and mortality, is pathologically characterized by multi-organ dysfunction, with pulmonary involvement predominating as acute lung injury (ALI) or its severe progression to acute respiratory distress syndrome. Contemporary therapeutic strategies exhibit limited efficacy, while traditional Chinese medicine (TCM) grounded in millennia of clinical empiricism demonstrates unique pharmacological advantages through multi-component and multi-target regulation.</p><p><strong>Summary: </strong>The mechanism underlying sepsis-induced ALI centers on dysregulated inflammatory response, redox imbalance, and coagulopathy. This review systematically evaluates the effectiveness, mechanism, and clinical research progress of eight TCM formulas in the treatment of sepsis and ALI. Accumulating fundamental research and clinical trials demonstrate the potential of these TCM formulas in treating sepsis-induced ALI. The challenges and opportunities of TCM formulas in treating, including but not limited to, sepsis-induced ALI were emphasized.</p><p><strong>Key message: </strong>This review bridges traditional therapeutic wisdom with modern pathogenesis understanding, offering novel combinatorial strategies for sepsis-induced ALI management.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"360-374"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}