Biomolecules & biomedicine最新文献

{"title":"The association of plasma homocysteine levels with short-term mortality in sepsis patients: A meta-analysis.","authors":"Xinxing Lu, Xueyan Yuan, Yali Chao, Xiao Wu, Airan Liu","doi":"10.17305/bb.2024.11259","DOIUrl":"10.17305/bb.2024.11259","url":null,"abstract":"<p><p>The association between plasma homocysteine (Hcy) levels and short-term mortality in sepsis patients remains unclear. This meta-analysis aimed to clarify this potential relationship. Following PRISMA 2020 and Cochrane Handbook guidelines, we conducted a comprehensive literature search in the PubMed, Embase, and Web of Science databases up to June 24, 2024. We included cohort studies that assessed the association between plasma Hcy levels and all-cause mortality in adult sepsis patients. Standardized mean differences (SMDs) and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using a random-effects model to account for potential heterogeneity. Nine cohort studies involving 771 sepsis patients were included. Overall, no significant difference in plasma Hcy levels was observed between survivors and non-survivors (SMD: -0.23, 95% CI: -0.84 to 0.37, P = 0.45), with substantial heterogeneity (I² = 86%). Subgroup analysis revealed lower plasma Hcy levels among survivors in Chinese patients (SMD: -1.56, 95% CI: -1.98 to -1.13, P < 0.001) but not in non-Asian patients. Plasma Hcy levels were not significantly associated with all-cause mortality (OR per 1-unit increment: 1.03, 95% CI: 0.95 to 1.11, P = 0.51), with notable heterogeneity (I² = 72%). However, a significant association was found in Chinese patients (OR: 1.09, 95% CI: 1.03 to 1.15, P = 0.003), but not in non-Asian patients. In conclusion, plasma Hcy levels were not generally associated with short-term mortality in sepsis patients. However, significant associations were observed in Chinese patients, suggesting potential ethnic differences that warrant further investigation.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"786-797"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142559617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic immune-inflammation index and the short-term mortality of patients with sepsis: A meta-analysis.","authors":"Lingbo Liang, Qiaoli Su","doi":"10.17305/bb.2024.11494","DOIUrl":"10.17305/bb.2024.11494","url":null,"abstract":"<p><p>The systemic immune-inflammation index (SII) is a novel biomarker that reflects the balance between the host immune response and inflammation, two key pathophysiological processes involved in sepsis. This meta-analysis aimed to evaluate the relationship between SII at admission and short-term mortality in patients with sepsis. Literature searches were performed in PubMed, Embase, Web of Science, CNKI, and Wanfang up to August 30, 2024, using relevant search terms. Observational studies that reported the association between SII and short-term mortality in sepsis patients were included. Risk ratios (RRs) and 95% confidence intervals (CIs) comparing the incidence of mortality within 90 days in patients with sepsis with a high versus low SII were calculated. Nine cohort studies, with a total of 25,626 patients, were included. A high SII at admission was significantly associated with an increased risk of all-cause short-term mortality in sepsis patients (RR: 1.51, 95% CI: 1.31-1.67, P < 0.001), with moderate heterogeneity (I² = 43%). Sensitivity analyses confirmed the robustness of these findings. Subgroup analyses suggested a stronger association in patients younger than 67 years compared to those aged 67 years or older (P = 0.04), but no significant differences were observed based on sex, SII cutoff values, or follow-up duration. In conclusion, this meta-analysis demonstrates that elevated SII at admission is associated with an increased risk of short-term mortality in sepsis patients, particularly in younger individuals. Further research is needed to validate these findings and explore their clinical implications.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"798-809"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol 7 alpha-hydroxylase (<i>CYP7A1</i>) gene polymorphisms are associated with increased LDL-cholesterol levels and the incidence of subclinical atherosclerosis.","authors":"Gilberto Vargas-Alarcón, Rosalinda Posadas-Sánchez, Oscar Peréz-Méndez, José Manuel Fragoso","doi":"10.17305/bb.2024.10764","DOIUrl":"10.17305/bb.2024.10764","url":null,"abstract":"<p><p>The cholesterol 7 alpha-hydroxylase (CYP7A1) enzyme plays an important role in the conversion of cholesterol to bile acid, contributing to the reduction of cholesterol plasma levels in normal conditions. Nonetheless, recent studies have shown that some genetic variants in the enhancer and promoter regions of the CYP7A1 gene reduce the expression of the CYP7A1 enzyme, increasing plasma lipid levels, as well as the risk of developing coronary heart disease. The aim of this work was to explore whether the genetic variants (rs2081687, rs9297994, rs10107182, rs10504255, rs1457043, rs8192870, and rs3808607) of the CYP7A1 gene are involved in subclinical atherosclerosis and plasma lipid levels. We included 416 patients with subclinical atherosclerosis (SA) with coronary artery calcium (CAC) greater than zero, and 1046 controls with CAC = 0. According to the inheritance models (co-dominant, dominant, recessive, over-dominant and additive), the homozygosity of the minor allele frequencies of 7 analyzed polymorphisms showed a high incidence of SA (P < 0.05). In a sub-analysis performed including only the patients with SA, the same SNPs were associated with increased low-density lipoprotein cholesterol (LDL-C) levels. On the other hand, our findings showed that the haplotype (TGCGCTG) increases the risk of developing SA (P < 0.05). In conclusion, the rs2081687, rs9297994, rs10107182, rs10504255, rs1457043, rs8192870, and rs3808607 polymorphisms of CYP7A1 confer a risk of developing SA and elevated LDL-C levels. Our results suggest that the CYP7A1 is involved in the incidence of SA through the increase in the plasma lipid profile.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"822-832"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142115549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic accuracy of two-dimensional shear wave elastography and point shear wave elastography in identifying different stages of liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease: A meta-analysis.","authors":"Xiangyi Xu, Yiqing Zhang, Qiwei Zhu, Yuchen Xie, Yuanyuan Zhou, Bingtian Dong, Chaoxue Zhang","doi":"10.17305/bb.2024.11577","DOIUrl":"10.17305/bb.2024.11577","url":null,"abstract":"<p><p>To assess the diagnostic accuracy of two-dimensional shear wave elastography (2-D SWE) and point shear wave elastography (pSWE) in detecting liver fibrosis stages in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), a comprehensive search was conducted across four databases up to February 9, 2024. A bivariate random-effects model was used to analyze the diagnostic accuracy of the methods. After screening, 13 studies involving pSWE included 1527 patients, while nine studies involving 2-D SWE included 1088 patients. The areas under the summary receiver operating characteristic (SROC) curves for diagnosing significant fibrosis (F ≥ 2), advanced fibrosis (F ≥ 3), and cirrhosis (F = 4) using pSWE and 2-D SWE were as follows: 0.84 (95% CI 0.80-0.87), 0.91 (95% CI 0.88-0.93), and 0.94 (95% CI 0.91-0.95) for pSWE; 0.83 (95% CI 0.79-0.86) 0.85 (95% CI 0.82-0.88), and 0.89 (95% CI 0.86-0.91) for 2-D SWE, respectively. The pooled sensitivity for pSWE and 2-D SWE for stages F ≥ 2, F ≥ 3, and F = 4 were 0.71 (95% CI 0.63-0.78), 0.81 (95% CI 0.72-0.88), and 0.81 (95% CI 0.63-0.91) for pSWE, and 0.77 (95% CI 0.68-0.84), 0.80 (95% CI 0.72-0.87), and 0.92 (95% CI 0.75-0.98) for 2-D SWE, respectively. The pooled specificity of pSWE and 2-D SWE for these stages were 0.83 (95% CI 0.76-0.88), 0.87 (95% Cl: 0.81-0.92), and 0.91 (95% CI 0.86-0.94) for pSWE, and 0.76 (95% CI 0.66-0.84), 0.76 (95% CI 0.69-0.82), and 0.83 (95% CI 0.78-0.85) for 2-D SWE, respectively. In conclusion, both 2-D SWE and pSWE demonstrated high diagnostic performance in identifying various stages of liver fibrosis in MASLD patients.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"810-821"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial intelligence driven innovations in biochemistry: A review of emerging research frontiers.","authors":"Mohammed Abdul Lateef Junaid","doi":"10.17305/bb.2024.11537","DOIUrl":"10.17305/bb.2024.11537","url":null,"abstract":"<p><p>Artificial intelligence (AI) has become a powerful tool in biochemistry, greatly enhancing research capabilities by enabling the analysis of complex datasets, predicting molecular interactions, and accelerating drug discovery. As AI continues to evolve, its applications in biochemistry are poised to expand, revolutionizing both theoretical and applied research. This review explores current and potential AI applications in biochemistry, with a focus on data analysis, molecular modeling, enzyme engineering, and metabolic pathway studies. Key AI techniques-such as machine learning algorithms, natural language processing, and AI-based molecular modeling-are discussed. The review also highlights emerging research areas benefiting from AI, including personalized medicine and synthetic biology. The methodology involves an extensive analysis of existing literature, particularly peer-reviewed studies on AI applications in biochemistry. AI-driven tools like AlphaFold, which have significantly advanced protein structure prediction, are evaluated alongside AI's role in expediting drug discovery. The review also addresses challenges such as data quality, model interpretability, and ethical considerations. Results indicate that AI has expanded the scope of biochemical research by facilitating large-scale data analysis, enhancing molecular simulations, and opening new avenues of inquiry. However, challenges remain, particularly in data handling and ethical concerns. In conclusion, AI is transforming biochemistry by driving innovation and expanding research possibilities. Future advancements in AI algorithms, interdisciplinary collaboration, and integration with automated techniques will be crucial to fully unlocking AI's potential in advancing biochemical research.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"739-750"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The gut microbiota modulates airway inflammation in allergic asthma through the gut-lung axis related immune modulation: A review.","authors":"Meng Zhang, Ziwen Qin, Chuanjun Huang, Bin Liang, Xiuqing Zhang, Weitao Sun","doi":"10.17305/bb.2024.11280","DOIUrl":"10.17305/bb.2024.11280","url":null,"abstract":"<p><p>The human gut microbiota is a vast and complex microbial community. According to statistics, the number of bacteria residing in the human intestinal tract is approximately ten times that of total human cells, with over 1000 different species. The interaction between the gut microbiota and various organ tissues plays a crucial role in the pathogenesis of local and systemic diseases, exerting a significant influence on disease progression. The relationship between the gut microbiota and intestinal diseases, along with its connection to the pulmonary immune environment and the development of lung diseases, is commonly referred to as the \"gut-lung axis.\" The incidence of bronchial asthma is rising globally. With ongoing research on gut microbiota, it is widely believed that intestinal microorganisms and their metabolic products directly or indirectly participate in the occurrence and development of asthma. Based on the gut-lung axis, this review examines recent research suggesting that the intestinal microbiota can influence the occurrence and progression of allergic asthma through the modulation of cytokine immune balance and mucosal integrity. Though the precise immune pathways or microbial species influencing asthma through the gut-lung axis are still under exploration, summarizing the immune modulation through the gut-lung axis in allergic asthma may provide insights for the clinical management of the condition.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"727-738"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Piezo1-driven mechanotransduction as a key regulator of cartilage degradation in early osteoarthritis.","authors":"Xu Yan, Su Fu, Ying Xie, Chunlin Zhang, Xuejian Wu","doi":"10.17305/bb.2024.11156","DOIUrl":"10.17305/bb.2024.11156","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a prevalent degenerative disease characterized by pain and cartilage damage in its later stages, while early OA is marked by the loss of cartilage's mechanical function. Recent studies suggest that Piezo1, a mechanotransducer, may contribute to cartilage degradation under abnormal physical stress. This study investigates the mechanism by which Piezo1 mediates the loss of cartilage's mechanical properties. Using rat chondrocytes cultured in a 3D in vitro model, we found that fluid flow-induced physical stress activates constitutively expressed Piezo1, leading to increased catabolic activity and apoptosis, which, in turn, disrupts the matrix structure. Ex vivo cartilage experiments further demonstrated that the mechanical stress-induced loss of cartilage's physical properties (approximately 10% reduction in relaxation modulus) is mediated by Piezo1 and depends on cell viability. Notably, Piezo1 agonists alone did not alter the mechanical behavior of cartilage tissue. In vivo, using an OA rat model induced by anterior cruciate ligament transection, we observed cartilage integrity degradation and loss of mechanical properties, which were partially mitigated by Piezo1 inhibition. RNA sequencing revealed significant modulation of the PI3K signaling and matrix regulation pathways. Collectively, this study demonstrates that Piezo1-mediated catabolic activity in chondrocytes is a key driver of the loss of cartilage's mechanical function during the relaxation phase.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"905-913"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin regulates sensitivity to X-ray radiation of hepatocellular carcinoma through miR-216a-3p.","authors":"Nuran Bedolla, Linyu Liu, Qiuxian Xie, Xueting Liu, Yanli Ren","doi":"10.17305/bb.2024.11125","DOIUrl":"10.17305/bb.2024.11125","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a highly aggressive liver cancer with limited therapeutic options, and enhancing radiosensitivity remains a key challenge in improving treatment outcomes. Quercetin (Que) can inhibit the progression of HCC; however, its effect on HCC radiosensitivity remains unclear. This research investigates the role of Que in regulating HCC growth and radiosensitivity, aiming to provide a scientific foundation for enhancing the clinical efficacy of radiation therapy in HCC. The CCK-8 assay was used to determine the optimal treatment conditions for Que and X-rays. Changes in cell growth, cycle arrest, invasion, migration, the relative proportion of JC-1 red and green fluorescence (mitochondrial membrane potential), and the levels of ROS, malondialdehyde, superoxide dismutase, and glutathione peroxidase (oxidative stress) were assessed using flow cytometry, Transwell assays, JC-1 staining, Western blot, and ELISA, respectively, under Que, X-ray, and co-treatment conditions. The effect of miR-216a-3p knockdown on the action of Que was also explored, and the potential pathways by which Que regulates HCC growth and radiosensitivity were investigated in conjunction with in vivo subcutaneous transplantation tumor experiments. The in vitro treatment parameters for Que and X-rays were 100 μM and 4 Gy. Que combined with X-ray therapy enhanced HCC cell radiosensitivity, reduced proliferation, invasion, and migration, and promoted oxidative stress and apoptosis. Que was found to upregulate miR-216a-3p in HCC cells. Rescue experiments with miR-216a-3p knockdowns demonstrated that Que regulates HCC cell radiosensitivity via miR-216a-3p. In vivo research further showed that Que increased tumor sensitivity to X-rays by upregulating miR-216a-3p, thereby inhibiting HCC growth. In conclusion, Que has been shown to enhance HCC radiosensitization by upregulating miR-216a-3p and inhibiting HCC progression. Que may be a promising agent for increasing the radiosensitivity of HCC.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"833-849"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142607549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and mechanisms of curcumin in the treatment of osteoarthritis: A scoping review.","authors":"Xiaodong Ma, Wenjian Zhao, Fan Yang, Kok-Yong Chin","doi":"10.17305/bb.2024.11045","DOIUrl":"10.17305/bb.2024.11045","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a degenerative joint disease that primarily affects the elderly worldwide. It is characterized by local inflammation, which can be targeted therapeutically using natural anti-inflammatory compounds such as curcumin. This scoping review explores the therapeutic effects and mechanisms of curcumin in OA management. A total of 50 relevant original studies published in English were selected from PubMed, Web of Science, and Scopus using specific search strings, regardless of study type. These studies demonstrated curcumin's anti-inflammatory, protective, and anti-apoptotic effects on chondrocytes. Curcumin has been shown to stimulate chondrocyte proliferation and collagen production while inhibiting matrix metalloproteinase activity. These mechanisms contribute to curcumin's ability to alleviate pain and improve joint function in OA patients. While the findings highlight curcumin's potential in OA management, further research is needed to enhance its bioavailability and determine optimal formulations, dosages, and administration routes.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"761-785"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HLA-DRB1*01 predicts treatment outcome in juvenile idiopathic arthritis: A retrospective-prospective cohort study.","authors":"Adisa Čengić, Sniježana Hasanbegović, Izeta Hamza, Tarik Suljić, Velma Selmanović, Aida Đozo, Elma Fejzić, Lamija Zečević-Pašić, Nejra Džananović","doi":"10.17305/bb.2024.11043","DOIUrl":"10.17305/bb.2024.11043","url":null,"abstract":"<p><p>Juvenile idiopathic arthritis (JIA) is the most common chronic inflammatory autoimmune disease in childhood, significantly contributing to both short- and long-term disability. While certain human leukocyte antigen (HLA) class II alleles are known to be associated with specific subgroups of JIA, emerging evidence suggests a strong correlation between these alleles and treatment response. This study involved 143 JIA patients diagnosed according to International League of Associations for Rheumatology criteria. Each patient underwent HLA class II typing, including HLA-B27, as well as tests for rheumatoid factor (RF) and antinuclear antibodies (ANA). Comprehensive rheumatological assessments were conducted at diagnosis, with follow-ups at three and six months post-onset. After six months of methotrexate (MTX) treatment, patients were categorized as responders or non-responders. Responders achieved clinically inactive disease based on the American College of Rheumatology Provisional Criteria for Defining Clinical Inactive Disease and Clinical Remission. Non-responders, who did not reach clinically inactive disease after six months of treatment, required the addition of another non-biological disease-modifying antirheumatic drug (DMARD) or a biological DMARD. Our analysis revealed that the HLA-DRB1*01 allele is a significant prognostic marker for therapeutic response, predicting therapeutic resistance (P=0.01). The most prevalent HLA-DRB1 alleles in the treatment-resistant group were HLA-DRB1*08:11 (11.3%), HLA-DRB1*01:01 (8.5%), HLA-DRB1*01:13, HLA-DRB1*04:11 (7%), HLA-DRB1*08:13, and HLA-DRB1*08:15 (4.2%). These findings highlight the critical role of HLA class II alleles in pediatric rheumatology, particularly in relation to treatment response and disease prognosis. In the era of personalized medicine, understanding the genetic contributions to treatment response and outcomes in JIA patients is essential. A key limitation of this study was the lack of comparison of treatment responses across different JIA subtypes. Future studies should prioritize evaluating MTX efficacy within specific JIA subgroups to enable a more tailored understanding of its effectiveness.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"883-893"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142559615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}