International Journal of Medical Sciences最新文献

{"title":"Health-Related Quality of Life in Patients with Hepatocellular Carcinoma Post-Surgery: A Scoping Review.","authors":"Wei-Zheng Zhang, Kok-Yong Chin, Roshaya Zakaria, Nor Haty Hassan","doi":"10.7150/ijms.115946","DOIUrl":"10.7150/ijms.115946","url":null,"abstract":"<p><p><b>Background</b>: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. While surgical treatments, including liver resection and transplantation, offer curative potential, they significantly impact patients' health-related quality of life (HRQoL). This scoping review aims to comprehensively map the existing literature on HRQoL following surgical treatment for HCC by identifying commonly used assessment tools, variations across surgical approaches, and key influencing factors. <b>Methods</b>: A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science from inception to February 2025, adhering to the Joanna Briggs Institute (JBI) Scoping Review methodology and the PRISMA-ScR checklist. Studies were included if they assessed post-operative HRQoL in HCC patients using validated instruments. Two independent reviewers screened, selected, and extracted data from eligible studies. <b>Results</b>: Of the 1,275 articles retrieved, 13 met the inclusion criteria. Sample sizes ranged from 66 to 332, with studies included conducted in the USA, China, Germany, Spain, Egypt, and Japan. The most frequently used HRQoL assessment tools were SF-36, FACT-Hep, and EORTC QLQ-C30. Findings revealed an initial decline in HRQoL postoperatively, followed by gradual recovery over 3-12 months. Liver transplantation generally resulted in substantial long-term HRQoL compared to liver resection, although challenges associated with immunosuppressive therapy persisted. Key factors influencing HRQoL included preoperative depression, post-operative complications, disease recurrence, and socioeconomic variables such as age, gender, and family support. <b>Conclusions</b>: Post-operative HRQoL in HCC patients follows a dynamic trajectory, which emphasizes the need for patient-centered care strategies. Standardized HRQoL assessments and longitudinal studies are crucial for enabling cross-study comparisons and guiding targeted interventions to optimize recovery and long-term well-being.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3709-3721"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular Endothelial Protection Effects of <i>Curcuma wenyujin</i> Root Aqueous Extracts on LPS-induced Rat Vascular Damage.","authors":"Li-Hsien Chen, Sheau-Chung Tang, Shu-Er Yang, Erl-Shyh Kao","doi":"10.7150/ijms.112103","DOIUrl":"10.7150/ijms.112103","url":null,"abstract":"<p><p>Sepsis caused by bacterial infection can also induce vascular endothelial damage through endotoxins secreted by bacteria such as lipopolysaccharides (LPS). The mechanism of LPS induce vascular endothelial damage is mainly through the release of pro-inflammatory factors and activation of matrix metalloproteinases (MMPs), then MMPs further cause the glycocalyx layer to damage endothelial cells and finally lead to hyperosmolar vascular abnormalities and eventually microcirculatory disorders in general clinical practice, and are used in clinical treatment to prevent the release of pro-inflammatory factors. However, the immunosuppressive effect of high-dose dexamethasone is unpredictable before pathogens are cleared. <i>Curcuma wenyujin</i> (CW) is a traditional Chinese medicine containing the biologically active ingredient β-elemene, which has been reported to have endothelial protective effects. In this study, an acute vascular endothelial damage animal model was established by intraperitoneal injection of LPS in rats, and the treatments included oral administration of CW root aqueous extract solution at a low dose (LW group, 375 mg/kg/day) and high dose (HW group, 1500 mg/kg) for endothelial protection evaluation. The results demonstrated that HW reduced the TLR4 signaling pathway and downstream markers of vascular inflammation, particularly MMP2 and MMP9. This study suggests that CW, a traditional Chinese medicine, could CW root aqueous extracts treatments protect against LPS-induced acute vascular damage in rats. This study advocates for further clinical exploration of CW as a potential clinical use in bacterial infection-induced sepsis or complementary treatment to current therapies, potentially benefiting cardiovascular and other inflammatory conditions.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3556-3564"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C-C chemokine receptor type 5 activation stimulates adipocyte differentiation through ERK-dependent pathway.","authors":"Luen-Kui Chen, Chien-Wei Chen, Shao-Yun Wu, Shui-Yu Liu, Liang-Yi Wu, Chi-Jen Chang, Leticia B Sy, Chi-Chang Juan","doi":"10.7150/ijms.115524","DOIUrl":"10.7150/ijms.115524","url":null,"abstract":"<p><p>Obesity is associated with low-grade chronic inflammation, and research has shown that RANTES and CCR5 mRNA levels are notably higher in the visceral adipose tissue of obese individuals compared to lean controls. However, the precise role of CCR5 activation in obesity development is still unclear. This study aims to explore the impact of CCR5 activation on adipogenesis and the underlying regulatory mechanisms. The study used 3T3-F442A preadipocytes and primary preadipocytes from wild-type (WT) and CCR5 knockout (CCR5^-/-) mice to assess the role of CCR5 activation in adipocyte differentiation. To investigate the <i>in vivo</i> effects of CCR5 on obesity, male C57BL/6J WT and CCR5^-/- mice were fed either a normal chow (NC) or a high-fat diet (HFD) for two months. Plasma RANTES levels, fat pad weight, adipocyte size, and adipose CCR5 expression were measured. Treatment with RANTES resulted in increased intracellular triglyceride accumulation and enhanced expression of adipogenic transcription factors such as PPARγ, C/EBPα, and the adipocyte-specific protein aP2 during differentiation. These findings suggest that RANTES facilitates adipocyte differentiation. Moreover, pretreatment with the CCR5 inhibitor maraviroc and the ERK inhibitor PD98059 significantly reduced RANTES-induced adipocyte differentiation. RANTES also promoted differentiation in primary preadipocytes from WT mice, but not from CCR5^-/- mice. <i>In vivo</i>, WT mice on a high-fat diet showed higher plasma RANTES levels and increased adipose CCR5 expression, as well as obesity, whereas these changes were absent in CCR5^-/- mice. The results suggest that CCR5 activation by RANTES enhances adipocyte differentiation via an ERK-dependent pathway, and that CCR5 plays a critical role in the development of obesity.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3490-3500"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-6126 modulates GRP78 to suppress the Warburg effect and mitochondrial dynamics in triple-negative breast cancer.","authors":"Wei-Jan Wang, Jian-Sheng Liu, Nguyen Hoang Anh Kha, Wan-Jou Shen, Chih-Jung Chen, Shuan-Chu Chen, Pin-Chen Liao, Chih-Yang Huang, Wei-Wen Kuo","doi":"10.7150/ijms.107240","DOIUrl":"10.7150/ijms.107240","url":null,"abstract":"<p><p>Cancer cells often exhibit a metabolic shift towards aerobic glycolysis, known as the Warburg effect, leading to excessive energy production that facilitates tumorigenesis, including in breast cancer. Recently, non-coding RNAs, including microRNAs (miRNAs), have been identified as playing crucial roles in various human cancers. However, their roles in regulating metabolic reprogramming in breast cancer remain largely unexplored. Here, we identified the novel miRNA miR-6126, which is highly expressed in TNBC cells by using a miRNA microarray analysis. Overexpression of miR-6126 reduced the growth of TNBC cells and induced apoptosis by targeting GRP78 <i>in vitro</i> and <i>in vivo</i>. In addition, a luciferase reporter assay confirmed that GRP78 is a direct target of miR-6126. Elevated glucose metabolism, indicated by increased levels of LDHA and glucose transporter-1, was observed in TNBC following GRP78 overexpression. Treatment with miR-6126 mimics or GRP78 siRNA not only reduced LDHA and GLUT1 expression but also decreased glucose uptake and lactate release in TNBC cells. Moreover, miR-6126 impaired mitochondrial function by inducing mitochondrial fission through the downregulation of phospho-Drp1 (Ser616) and FIS1. Furthermore, we demonstrated that the expression of miR-6126 is negatively correlated with GRP78 in human tumor tissues. Our findings revealed that miR-6126 is implicated in tumorigenesis via the Warburg effect by targeting GRP78 and restoring mitochondrial function in TNBC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3598-3616"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Gut Microbiota and Pneumonia Risk: A Systematic Review and Mendelian Randomization.","authors":"Qingping Deng, Yuanyuan Liu, Hui Rong, Qing Liu, Rongyuan Yang","doi":"10.7150/ijms.114372","DOIUrl":"10.7150/ijms.114372","url":null,"abstract":"<p><p><b>Background:</b> The gut-lung axis represents a critical pathway potentially modulating COVID-19 pathogenesis. We employed meta-analysis to investigate the Mendelian randomization (MR) studies for the putative causal relationships between gut microbiota composition/metabolites and COVID-19 severity. <b>Methods:</b> Adhering to PRISMA 2020 guidelines, we conducted a systematic review of MR studies (PubMed/Web of Science/Embase/Scopus/Cochrane; inception to June 2024). Data from 11 studies (aggregating 32,748,274 participants; 1,487 SNPs) underwent meta-analysis across four COVID-19 severity strata including susceptibility, infection, hospitalization, and critical disease. Study quality was evaluated using a validated MR framework assessing 32 core assumptions. <b>Results:</b> Elevated COVID-19 susceptibility risk was associated with <i>Actinobacteria</i> (OR 1.16, 95% CI 1.06-1.26) and <i>Negativicutes</i> (1.06, 1.03-1.09), whereas protective effects emerged for <i>Oxalobacter</i> (0.84, 0.71-0.99) and <i>Ruminococcaceae UCG014</i> (0.88, 0.78-0.99). For COVID-19 infection, <i>Negativicutes</i> conferred increased risk (1.13, 1.02-1.26), while the <i>Ruminococcus</i> torques group (0.54, 0.39-0.74) and <i>Parasutterella</i> (0.90, 0.83-0.97) demonstrated protection. Hospitalization risk elevated with <i>MollicutesRF9</i> (1.13, 1.04-1.22) and <i>Alloprevotella</i> (1.25, 1.07-1.45), contrasting with <i>butyrate</i> (0.97, 0.94-0.99) and <i>Ruminiclostridium</i>6 (0.81, 0.69-0.94) showing protective associations. Severe COVID-19 risk increased with <i>Actinobacteria</i> (1.20, 1.01-1.42), <i>Bifidobacterium</i> (2.09, 1.15-3.81), and <i>Alloprevotella</i> (1.66, 1.36-2.01), while <i>Oxalobacter</i> (0.84, 0.76-0.92) and <i>Subdoligranulum</i> (0.82, 0.76-0.89) exhibited protection. Notably, <i>Actinobacteria</i>, <i>Negativicutes,</i> and <i>Alloprevotella</i> constituted consistent risk factors across severity strata, whereas <i>Oxalobacter</i> and <i>Parasutterella</i> showed trans-stage protective effects. <i>Butyrate</i> production specifically attenuated hospitalization risk, and <i>Bifidobacterium</i> demonstrated strikingly elevated critical disease risk, contrasting with typical probiotic associations. <b>Conclusions:</b> This meta-analysis of MR studies provides robust evidence for severity-specific causal effects of the gut microbiota on COVID-19 outcomes. The identified microbial taxa and metabolites provide potential biomarkers for clinical risk stratification and targets for novel adjuvant therapeutic strategies.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3511-3527"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal Stem Cells Senescence: Mechanism and Rejuvenation Interventions.","authors":"Qinghong Meng, Yan Zheng, Xiaobo Chen, Jiawei Mu, Changlin Li, Yiwen Gao, Wei Liu, Yuliang Wang","doi":"10.7150/ijms.115650","DOIUrl":"10.7150/ijms.115650","url":null,"abstract":"<p><p>Aging has become one of the most significant challenges and burdens on public health and healthcare systems worldwide. However, it is possible to slow down the aging process through various interventions. Mesenchymal stromal/stem cells (MSCs) have emerged as one of the most promising therapeutic agents for combating aging and treating various age-related chronic medical conditions. This is primarily due to their well-known cellular plasticity and potent multipotency, which enable them to promote tissue repair and regeneration, as well as address inflammatory conditions. Remarkably, the high quality and functional activity of MSCs are negatively affected by cellular senescence, particularly in both healthy-aging MSCs and replicative senescent MSCs. This is a critical issue when considering the provision of \"personalized\" or \"universal\" clinical-grade products. Therefore, this review aims to summarize the biological properties, immunomodulatory dysfunction, and underlying mechanisms of senescent MSCs. Additionally, it discusses the current promising techniques published for rejuvenating senescent MSCs and optimizing their therapeutic potential.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3692-3708"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The application of hyaluronic acid-containing artificial tears on the ocular surface of children receiving orthokeratology contact lens treatment.","authors":"Chia-Yi Lee, Shun-Fa Yang, Jing-Yang Huang, Chao-Kai Chang","doi":"10.7150/ijms.113380","DOIUrl":"10.7150/ijms.113380","url":null,"abstract":"<p><p><b>Purpose:</b> The purpose of this study was to compare the effects of the application of hyaluronic acid (HA)-containing artificial tears and non-HA artificial tears on the ocular surface of children receiving orthokeratology contact lens treatment. <b>Method:</b> Charts of patients fitted with orthokeratology contact lenses in any of 20 local clinics were reviewed in this retrospective cohort study. The patients were then categorized according to the artificial tear type used, resulting in 85 and 95 patients being placed into the non-HA and HA groups, respectively. The primary outcomes include fluorescein ocular surface staining and dry eye disease (DED)-related symptoms which were measured at 1, 3 and 6 months after orthokeratology contact lens treatment. An independent t test and Chi-square test were used for statistical analysis. <b>Results:</b> At one month, there was a statistically significant greater number of non-HA patients with staining (14 non-HA, 4 HA, P=0.017). In the final visit, the incidence of ocular surface stain was also significantly lower in the HA group (12 non-HA, 2 HA, P = 0.010). At one month, there was a statistically significant greater number of non-HA patients with DED-related symptoms (24 non-HA, 12 HA, P = 0.029). Finally, the number of DED-related symptoms was significantly lower in the HA group (P = 0.005). After a 6-month follow-up, the spherical equivalent refraction (SER) and axial length (AXL) values between the two groups showed no significant difference (all P > 0.05). <b>Conclusions:</b> The application of HA-containing artificial tears resulted in less ocular surface staining and fewer DED-related symptoms in children wearing overnight orthokeratology contact lenses.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3591-3597"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Metabolic Abnormalities During the Progression of Chronic Kidney Disease and Preventive Strategies.","authors":"Dongqing Zha, Ping Gao, Xiaoyan Wu","doi":"10.7150/ijms.114382","DOIUrl":"10.7150/ijms.114382","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is characterized by persistent renal impairment or dysfunction that lasts for at least 3 months, and typically has a progressive and irreversible trajectory. The increasing prevalence of metabolic disorders, such as hyperuricemia, dyslipidemia, obesity, and type 2 diabetes mellitus, have contributed to the increasing incidence of CKD, and it is now a significant public health concern worldwide. Accumulating evidence underscores the intricate relationships of the different metabolic disorders and how they promote the initiation and progression of CKD, and ultimately lead to end-stage renal disease (ESRD). Metabolic abnormalities promote CKD progression by various mechanisms, including oxidative stress, chronic inflammation, dysregulation of autophagy, glomerular hyperfiltration and disruption of hemodynamics, endothelial dysfunction, and dysbiosis of gut microbiota. Ectopic lipid deposition and lipid peroxidation-induced redox imbalance lead to mitochondrial dysfunction, excessive production of reactive oxygen species (ROS), and activation of the p38 MAPK, ERK, and JNK signaling pathways. Metabolic dysregulation activates NF-κB signaling pathways and NLRP3 inflammasomes, leading to increased production of pro-inflammatory factors, lysosomal dysfunction, and impaired autophagic clearance, followed by accumulation of metabolic waste and podocyte injury. Obesity and hyperlipidemia can cause excessive activation of the renin-angiotensin-aldosterone system (RAAS), which then causes glomerular hyperfiltration, endothelial and mesangial cell injury and proliferation, and ultimately glomerulosclerosis. Multiple interventions that target these mechanisms have shown therapeutic potential, and these include pharmacological treatments (xanthine oxidase inhibitors to reduce uric acid levels, statins for lipid regulation, and SGLT2 inhibitors and GLP-1 receptor agonists to improve renal and cardiovascular outcomes), lifestyle interventions (low-salt and low-protein diets, weight management, smoking cessation, and alcohol limitation), intermittent fasting, and microbiome-targeted therapies. This review analyzes the pathways by which metabolic abnormalities affect the onset and progression of CKD, identifies strategies that have potential use for prevention or treatment, and offers a robust theoretical foundation for the future development of effective clinical interventions.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3543-3555"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galangin Mitigates Oxidative Damage Induced by Environmental Stresses in Skin Keratinocytes.","authors":"Herath Mudiyanselage Udari Lakmini Herath, Mei Jing Piao, Kyoung Ah Kang, Pincha Devage Sameera Madushan Fernando, Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna, Young Sang Koh, Eui Tae Kim, Suk Ju Cho, Jin Won Hyun","doi":"10.7150/ijms.112872","DOIUrl":"10.7150/ijms.112872","url":null,"abstract":"<p><p>Particulate matter 2.5 (PM_2.5) is a major air contaminant that causes skin damage by interacting with ultraviolet (UV) radiation. Exposure to those environmental stresses leads to oxidative skin damage and apoptosis. Although galangin is a natural flavonoid with antioxidant and several bioactive properties, its antioxidative effects following combined PM_2.5 and UVB exposure have not been fully investigated. Therefore, the aim of this study was to investigate the protective effect of galangin against PM_2.5- and UVB-induced oxidative stress and apoptosis in keratinocytes. Human HaCaT keratinocytes were pre-treated with galangin and treated with PM_2.5 and/or UVB. Intracellular reactive oxygen species (ROS) levels, lipid peroxidation, protein oxidation, DNA damage, mitochondrial damage, apoptotic protein expression, and cellular apoptosis were assessed using flow cytometry, confocal microscopy, and western blotting. Galangin reduced ROS levels, lipid peroxidation, protein oxidation, DNA damage, mitochondrial damage, and cellular apoptosis caused by PM_2.5 and/or UVB exposure. Additionally, galangin attenuated PM_2.5- and UVB-induced upregulation of apoptosis-related proteins and restored the expression of anti-apoptotic proteins. PM_2.5 and/or UVB enhanced cellular apoptosis by activating the mitogen-activated protein kinase (MAPK) signaling pathway. Notably, combined treatment with MAPK inhibitors and galangin demonstrated a protective effect against PM_2.5- and/or UVB-induced apoptosis. Galangin protected human keratinocytes against PM_2.5- and/or UVB-induced cellular damage by inhibiting MAPK signaling, suggesting that it may be a beneficial ingredient in skin care products designed to safeguard the skin from the detrimental effects of environmental stress.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3682-3691"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolism and Targeted Therapy of Fibrosis in Chronic Pancreatitis: A Review.","authors":"Hongqing Luo, Shan Guo, Yuning Chu, Yiping Xin, Xiaoyan Yin, Xiaoyu Li","doi":"10.7150/ijms.118338","DOIUrl":"10.7150/ijms.118338","url":null,"abstract":"<p><p>Chronic pancreatitis (CP) is a progressive condition characterized by persistent pancreatic inflammation, tissue destruction, and fibrosis. Recent studies have highlighted the crucial role of metabolic processes in the pathogenesis of pancreatic fibrosis, particularly the metabolic reprogramming of pancreatic stellate cells (PSCs) and immune cells. Disruptions in glucose, lipid, and amino acid metabolism have been shown to play a key role in the progression of CP fibrosis, exacerbating disease severity. Activated PSCs exhibit enhanced glycolysis and lipid metabolism, which promote excessive extracellular matrix (ECM) production and tissue remodeling. Simultaneously, immune cells such as macrophages and T cells undergo metabolic reprogramming, further intensifying inflammation and fibrosis. This review discusses the role of metabolic reprogramming in pancreatic fibrosis and proposes potential therapeutic strategies targeting metabolic pathways, including glycolysis inhibitors, lipid metabolism modulators, and amino acid metabolism regulators. These strategies offer promising prospects for mitigating the progression of CP fibrosis and provide new therapeutic avenues for clinical applications.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 14","pages":"3528-3542"},"PeriodicalIF":3.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}