Biologics : Targets & Therapy最新文献

{"title":"Telitacicept: A New Therapy for the Treatment of Optic Neuromyelitis Spectrum Disease Associated with Other Autoimmune Disorders.","authors":"Shaomin Zuo, Wenning Yang, Siyu Zhang, Shuyue Sun, Songke Lu, Chengcheng Lu, Wei Li","doi":"10.2147/BTT.S508605","DOIUrl":"10.2147/BTT.S508605","url":null,"abstract":"<p><p>Neuromyelitis optica spectrum disorders (NMOSD) are primarily autoimmune diseases mediated by B cells and AQP4-IgG antibodies, typically affecting the optic nerves and spinal cord, and are characterised by high relapse rates and significant disability. We present two cases of NMOSD patients who also had systemic lupus erythematosus (SLE), with one case additionally complicated by myasthenia gravis (MG). Both patients initially received first-line treatment with corticosteroids; however, no clinical improvement was observed; As a result, the treatment was switched to the dual-target biologic agent, Telitacicept. Following the administration of Telitacicept, both patients demonstrated significant improvements in clinical symptoms, daily functional abilities, and imaging findings. This report highlights the successful use of Telitacicept in treating NMOSD complicated by other autoimmune diseases, which may serve as an important reference for the management of NMOSD.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"149-155"},"PeriodicalIF":5.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating Biosimilar Development Projects: An Analytical Framework Utilizing Net Present Value.","authors":"Ranjit Ranbhor, Priyanka Kulkarni","doi":"10.2147/BTT.S514767","DOIUrl":"10.2147/BTT.S514767","url":null,"abstract":"<p><strong>Background: </strong>The increasing prominence of biosimilars in healthcare delivery has created the need for robust financial evaluation methods to assess development opportunities. Unlike traditional generic drugs, biosimilars require substantial investments ($100-250 million) and longer development timelines (6-8 years), necessitating sophisticated evaluation approaches.</p><p><strong>Methods: </strong>This study presents a comprehensive Net Present Value (NPV) analysis framework specifically designed for biosimilar development projects. Our framework incorporates key technical, regulatory, and commercial factors through a risk-adjusted NPV methodology, validated through case studies of three monoclonal antibody biosimilar development programs.</p><p><strong>Results: </strong>The analysis reveals that successful projects require minimum peak sales of $250-300 million to achieve a positive NPV, with market share and manufacturing efficiency serving as critical value drivers. Cost analysis shows that clinical development represents the largest share (57%) of total development costs.</p><p><strong>Conclusion: </strong>The framework demonstrates that early market entry, manufacturing optimization, and market share achievement are key success factors, whereas technical complexity and competitive intensity significantly influence risk-adjusted returns.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"125-135"},"PeriodicalIF":5.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet-Derived Growth Factor as Biomarker of Clinical Outcome for Autologous Platelet Concentrate Therapy in Grade I Knee Osteoarthritis.","authors":"Michele Francesco Di Tolla, Serena Romano, Pietro Vassetti, Domenico Perugini, Immacolata Filoso, Serena Cabaro, Giusy Ferraro, Francesco Oriente, Giuseppe Perruolo, Flora Arvonio, Vittoria D'Esposito, Pietro Formisano","doi":"10.2147/BTT.S500522","DOIUrl":"10.2147/BTT.S500522","url":null,"abstract":"<p><strong>Introduction: </strong>Autologous platelet concentrates (APC) are widely used in the infiltrative treatment of knee osteoarthritis (OA) to enhance tissue healing and relieve pain. Aim of this study was to identify predictive biomarkers for clinical outcomes in patients with grade I knee OA.</p><p><strong>Methods: </strong>A panel of growth factors (GFs) and cytokines was determined in peripheral blood (PB) and APC. The Numeric Pain Rating Scale (NPRS) was used as a clinical readout before and after the APC infiltration.</p><p><strong>Results: </strong>A lower white blood cell (WBC) count and higher Monocyte-chemoattractant Protein-1 levels in PB were associated with APC-induced pain relief. Platelet-derived Growth Factor (PDGF) levels in APC were significantly higher in OA patients displaying a larger NPRS reduction, independent of platelet count. Finally, the simultaneous determination of PDGF, Vascular Endothelial Growth Factor, and Macrophage Inflammatory Protein-1α in APC discriminated OA patients with very poor or no response.</p><p><strong>Conclusion: </strong>Platelet-released GFs rather than platelet counts may predict clinical outcomes in grade 1 knee OA.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"137-147"},"PeriodicalIF":5.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting DNA Topoisomerase IIα in Retinoblastoma: Implications in EMT and Therapeutic Strategies.","authors":"Qingquan Wei, Nan Lin, Li Wang","doi":"10.2147/BTT.S499314","DOIUrl":"10.2147/BTT.S499314","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the role of DNA topoisomerase IIα (TOP2A) in retinoblastoma (RB), focusing on its involvement in epithelial-mesenchymal transition (EMT) and the potential of TOP2A inhibition as a therapeutic strategy.</p><p><strong>Methods: </strong>We analyzed TOP2A expression in RB tissues using public gene expression databases (GSE97508, GSE110811, and GSE172170) and conducted functional assays in human RB cell lines (Y79 and WERI-Rb-1) modified to knock down or overexpress TOP2A. Assessments included cell proliferation, migration, invasion, and EMT marker expression via RT-PCR and Western blot. Additionally, we evaluated the effects of TOP2A modulation in subcutaneous and liver metastasis mouse xenograft models.</p><p><strong>Results: </strong>TOP2A was significantly overexpressed in RB tissues (p < 0.0001). In vitro, TOP2A knockdown inhibited RB cell proliferation, migration, and invasion, and reversed EMT marker expression (p < 0.05), while TOP2A overexpression enhanced these oncogenic processes. In vivo, TOP2A knockdown or inhibition significantly reduced tumor growth and metastasis in both subcutaneous and liver metastasis models (p < 0.05). Combination therapy with TOP2A and EMT inhibitors further enhanced anti-tumor effects, significantly reducing tumor burden and metastatic lesions (p < 0.01).</p><p><strong>Conclusion: </strong>TOP2A is pivotal in RB pathogenesis and progression, primarily by regulating EMT. Its inhibition not only curtails RB cell proliferation and metastasis but also reverses EMT, underscoring its potential as a therapeutic target. This study lays the groundwork for further exploration of TOP2A-targeted therapies in RB.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"113-123"},"PeriodicalIF":5.3,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Escalation and De-Escalation Strategies for Endocrine Therapy in Early-Stage Breast Cancer.","authors":"Tamer Al-Batsh, Nayef Abdel-Razeq, Yosra Al-Masri, Osama El-Khatib, Baha Sharaf, Faris Tamimi, Hikmat Abdel-Razeq","doi":"10.2147/BTT.S508634","DOIUrl":"10.2147/BTT.S508634","url":null,"abstract":"<p><p>Although adjuvant endocrine therapy (ET) greatly lowers the risk of recurrence and mortality in hormone receptor (HR)-positive early-stage breast cancer (EBC), more than 20% of patients may experience relapses within 10 years, often manifesting as incurable distant metastases. To improve outcomes, ovarian function suppression (OFS) with gonadotropin-releasing hormone agonists (GnRHa) added to tamoxifen or aromatase inhibitors like exemestane have shown significant disease-free survival (DFS) and, in some cases, overall survival (OS) benefits. CDK4/6 inhibitors, a cornerstone in metastatic HR-positive, HER2-negative breast cancer (MBC), are now being explored in EBC. Trials with abemaciclib and ribociclib have shown promise in high-risk EBC. For BRCA-mutant patients, the PARP inhibitor olaparib, as demonstrated in the OlympiA trial, significantly improved invasive DFS and OS when used as adjuvant therapy for one year. Conversely, de-escalation strategies are also emerging. Recent studies suggest that younger premenopausal women with low-risk disease may safely interrupt ET after 18-30 months to pursue pregnancy. Additionally, genomic tumor profiling is widely utilized to decide on aggressiveness of adjuvant therapy of EBC. These advancements reflect a shift toward personalized adjuvant therapy, integrating targeted treatments like CDK4/6 inhibitors and PARP inhibitors, optimizing ET with OFS, and balancing efficacy with quality of life through de-escalation strategies. This tailored approach aims to improve long-term outcomes for HR-positive EBC patients.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"97-111"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11913037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.","authors":"María J Sánchez-Quintero, Andrea Iboleón, Laura Martín Chaves, Bárbara Pozo Vilumbrales, Ada D M Carmona-Segovia, Pilar Martínez López, Miguel Romero-Cuevas, Jorge Rodríguez-Capitán, Víctor M Becerra-Muñoz, Francisco Javier Pavón-Morón, Mora Murri","doi":"10.2147/BTT.S504289","DOIUrl":"10.2147/BTT.S504289","url":null,"abstract":"<p><strong>Purpose: </strong>Aortic valve disease (AVD) is a common condition that leads to pressure and/or volume overload in the left ventricle. Aortic valve replacement is the standard treatment, as no pharmacological therapies are currently available. The incidence of AVD is increasing in developed countries, making the discovery of new biomarkers for early detection crucial. The importance of mitochondria in heart function is well established, and various cardiovascular pathologies are associated with mitochondrial dysfunction. In this cross-sectional study, we evaluated for the first time the role of mitochondria in AVD, aiming to identify new pathways involved in the disease and discover potential biomarkers.</p><p><strong>Patients and methods: </strong>We recruited 17 patients diagnosed with AVD and scheduled for aortic valve replacement, and 22 healthy controls. Plasma levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) and mitochondrial open reading frame of the 12S rRNA type-c peptide (MOTS-c) were measured by ELISA.</p><p><strong>Results: </strong>We observed significantly reduced levels of both proteins in patients, suggesting that substantial mitochondrial dysfunction occurs in AVD patients, independent of sex or age, but directly related to the disease.</p><p><strong>Conclusion: </strong>Mitochondria may represent a promising target for studying new pathways involved in AVD. We propose PGC1α and MOTS-c as potential plasma biomarkers for AVD detection. Further studies, including early-stage patients, are necessary to confirm the significance of our findings.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"87-96"},"PeriodicalIF":5.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanisms and Therapeutic Implications of PI3K Signaling in Airway Inflammation and Remodeling in Asthma.","authors":"Bangguo Song, Jihong Hu, Shupeng Chen, Yang Zhang","doi":"10.2147/BTT.S497622","DOIUrl":"10.2147/BTT.S497622","url":null,"abstract":"<p><p>Bronchial asthma is a complex and heterogeneous disease with ongoing airway inflammation and increased airway responsiveness. Key characteristics of the disease include persistent airway inflammation, airway hyperresponsiveness, and airway remodeling. Asthma's chronic and recurrent characteristics contribute to airway remodeling and inflammation, which can exacerbate lung damage. Presently, inflammation is predominantly managed with corticosteroids, yet there is a notable absence of treatments specifically addressing airway remodeling. The phosphoinositide 3-kinase (PI3K) signaling pathway is integral to the processes of inflammation, airway remodeling, and immune responses. Pharmacological agents targeting this pathway are currently undergoing clinical evaluation. This review elucidates the role of PI3K in the immune responses, airway inflammation, and remodeling associated with asthma, examining its underlying mechanisms. Furthermore, we synthesize the existing literature on the therapeutic potential of PI3K inhibitors for asthma management, emphasizing immune modulation, airway inflammation, and remodeling, including drug development and ongoing clinical trials. Lastly, we explore how various PI3K-targeted therapies may enhance efficacy and improve tolerance.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"73-86"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Anti-HER2 Therapy Vs Trastuzumab Alone with Neoadjuvant Anthracycline and Taxane in HER2-Positive Early-Stage Breast Cancer: Real-World Insights.","authors":"Baha Sharaf, Faris Tamimi, Haneen Al-Abdallat, Suhaib Khater, Osama Salama, Anas Zayed, Osama El Khatib, Assem Qaddoumi, Malek Horani, Yosra Al-Masri, Wafa Asha, Bayan Altalla', Hira Bani Hani, Hikmat Abdel-Razeq","doi":"10.2147/BTT.S468650","DOIUrl":"10.2147/BTT.S468650","url":null,"abstract":"<p><strong>Introduction: </strong>The integration of anti-HER2 targeted therapy with chemotherapy has demonstrated an increase in pathologic complete response rates (pCR) in patients with HER2-positive early-stage breast cancer (EBC). This study presents real-world data on the use of trastuzumab with or without pertuzumab, in combination with anthracycline and taxanes-based chemotherapy regimen.</p><p><strong>Methods: </strong>We conducted a retrospective analysis of patients with HER2-positive EBC who underwent neoadjuvant chemotherapy (NACT), treated between January 2014 and September 2021. The regimen included four cycles of doxorubicin and cyclophosphamide (AC), followed by four cycles of docetaxel every three weeks, with anti-HER2 therapy administered alongside docetaxel. Outcomes assessed included pCR, 3-year disease-free survival (DFS), and surgical outcomes.</p><p><strong>Results: </strong>During the study period, 484 consecutive patients with HER2-positive EBC, median age of 47 (range, 21-80) years, were enrolled. (64.7%) of patients received dual anti-HER2 therapy, while 35.3% received single-agent trastuzumab. The overall pCR rate was 44.2%, with a higher rate (55.6%) in hormone receptor (HR)-negative patients compared to HR-positive patients (39.8%), p=0.002. Although dual therapy resulted in a higher pCR rate (46.6%) compared to trastuzumab alone (39.8%), the difference was not statistically significant (p=0.15). The estimated 3-year DFS was 86.1% with dual therapy and 83.1% with trastuzumab alone (p=0.37). Further stratification revealed superior 3-year DFS in node-negative disease (96.4%) compared to node-positive disease (82.3%), p=0.0021. Patients who achieved pCR had a significantly better 3-year DFS (89.3%) compared to those with residual disease (82.2%), p=0.0177. Rate of breast conserving surgery (BCS) was lower (15.2%) among patients who received trastuzumab alone, compared to 26.5% among those who received dual anti-HER2 [Odds Ratio (OR)= 0.50, 95% Confidence Interval (CI), 0.30-0.80, p=0.005].</p><p><strong>Conclusion: </strong>Dual anti-HER2 therapy did not significantly enhance DFS but was associated with higher BCS rates, highlighting its potential to improve surgical outcomes.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"59-71"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling Tumor-to-Tumor Metastasis: Insights into Pathogenesis, Diagnostic Challenges, and Treatment Modalities.","authors":"Wennei Mei, Dongdong Zhang","doi":"10.2147/BTT.S505950","DOIUrl":"10.2147/BTT.S505950","url":null,"abstract":"<p><p>Tumor-to-tumor metastasis (TTM) is defined as the metastasis of one distinct malignancy to another independent tumor without directly extending into the substance of a histologically distinct and separate tumor. TTM is an extremely rare phenomenon that constitutes a very small percentage of all tumor metastases. The detailed histogenic mechanisms of TTM remain unclear. TTM is easily confused with composite tumors and synchronous tumors. Due to the rarity and complexity of the disease, it presents significant challenges in providing accurate diagnoses and appropriate treatment options. The exploration of TTM not only provides an in-depth understanding of the metastasis process, but also has significant implications for the management and treatment of patients with multiple primary malignant tumors, underscoring the necessity of comprehensive diagnostic and treatment strategies. The purpose of this review is to increase awareness of tumor-to-tumor metastasis, with a focus on pathogenesis, diagnosis, and treatment.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"43-58"},"PeriodicalIF":5.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine Intervention Mitigates Myocardial Ischemia-Reperfusion Injury in a Rat Model: Mechanistic Insights via miR-184 Signaling.","authors":"Haichen Yang, Gang Cao, Xia Li, Zhikun Zhao, Yong Wang, Fei Xu","doi":"10.2147/BTT.S479430","DOIUrl":"https://doi.org/10.2147/BTT.S479430","url":null,"abstract":"<p><strong>Background: </strong>Ischemia-reperfusion (I/R) injury is a major contributor to myocardial dysfunction and tissue damage. A natural alkaloid-Berberine having a wide range of pharmacological properties, has garnered interest for its potential cardioprotective properties. This study aimed to investigate the protective effects of berberine on myocardial tissue in a rat model of myocardial ischemia-reperfusion (I/R) injury. Additionally, the study explored the role of the miR-184/NOTCH1 signaling pathway in mediating these effects.</p><p><strong>Methods: </strong>Male Wistar rats were randomly assigned to five groups: sham-operated control, I/R injury, I/R treated with berberine, I/R treated with inhibitor NC and I/R treated with a miR-184 inhibitor. The I/R injury was induced by ligating the left anterior descending (LAD) coronary artery for 30 minutes, followed by 2 hours of reperfusion. Berberine was administered orally at 100 mg/kg/day for 2 weeks, and the miR-184 inhibitor was administered via intraperitoneal injection. Hemodynamic parameters were recorded using a pressure sensor connected to a catheter inserted into the left ventricle. Myocardial infarct size was assessed using TTC staining, while histological and molecular changes were evaluated through H&E staining, TUNEL assay, and Western blotting. The expression levels of target genes were analyzed using quantitative real-time PCR (qRT-PCR).</p><p><strong>Results: </strong>Berberine significantly reduced myocardial infarct size and improved hemodynamic parameters compared to the untreated I/R group. Additionally, berberine treatment attenuated apoptosis as evidenced by decreased TUNEL-positive cells. The miR-184 inhibitor also demonstrated protective effects by modulating key signaling pathways involved in myocardial injury. Western blot analysis revealed downregulation of NOTCH1 and HES1 expression in treated groups, indicating a potential mechanism for the observed cardio protection.</p><p><strong>Conclusion: </strong>Berberine and miR-184 inhibition offer significant protection against myocardial ischemia-reperfusion injury. These findings suggest that targeting miR-184 and associated pathways may be a promising therapeutic strategy for reducing cardiac damage following ischemia-reperfusion.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"19 ","pages":"31-42"},"PeriodicalIF":5.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11871928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}