{"title":"Macrophage Signaling Pathways in Health and Disease: From Bench to Bedside Applications","authors":"Yongquan Chi, Haipeng Jiang, Yiyuan Yin, Xinyu Zhou, Yiyouyou Shao, Yongsheng Li, Jianhua Rao","doi":"10.1002/mco2.70256","DOIUrl":"https://doi.org/10.1002/mco2.70256","url":null,"abstract":"<p>Macrophages exhibit remarkable functional plasticity by dynamically polarizing into proinflammatory or antiinflammatory subsets in response to microenvironmental cues. This duality underpins their pivotal roles in immune defense, tissue homeostasis, and disease progression; however, the molecular mechanisms governing their polarization and crosstalk across various pathologies remain incompletely defined. This review systematically delineates macrophage biology, emphasizing the interplay between subset-specific signaling networks and their context-dependent activation in both health and disease. The heterogeneity of macrophages is characterized by detailing the distinctions between tissue-resident and monocyte-derived origins, as well as their polarization states. Core pathways regulating phagocytosis, tissue repair, immune modulation, and neuroprotection are dissected, along with their dysregulation in autoimmune disorders, neurodegeneration, cancers, and cardiovascular diseases. Notably, microenvironmental factors such as damage-associated molecular patterns, pathogen-associated molecular patterns, and metabolic intermediates dynamically reshape macrophage phenotypes through NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activation or signal transducer and activator of transcription (STAT)-mediated transcriptional control. Preclinical and clinical evidence underscores potential therapeutic targets and emerging strategies. The significance of this review lies in its integrative analysis of signaling crosstalk, paradoxical pathway roles, and translational implications for precision therapies. These insights into macrophage functions and signaling pathways provide a robust foundation for future disease intervention and personalized medicine.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300213","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":"Autoimmune Diseases: Molecular Pathogenesis and Therapeutic Targets","authors":"Xiaoshuang Song, Hantian Liang, Fang Nan, Wenjing Chen, Junyao Li, Liu He, Yiping Cun, Zhenhong Li, Wei Zhang, Dunfang Zhang","doi":"10.1002/mco2.70262","DOIUrl":"https://doi.org/10.1002/mco2.70262","url":null,"abstract":"<p>Autoimmune diseases are a set of disorders in which the immune system attacks one's own tissues, leading to chronic inflammation, tissue damage, and systemic dysfunction. Affecting approximately 10% of the global population, these diseases impose significant health and economic burdens worldwide. The pathogenesis of autoimmune diseases is complex, involving not only genetic predisposition (e.g., human leukocyte antigen variants), environmental triggers (e.g., infections), and a dysregulated immune response but also various interacting components that contribute to the development of diverse clinical phenotypes. This review provides a comprehensive overview of common autoimmune diseases, covering their clinical manifestations, pathogenic mechanisms, and diagnostic approaches such as disease-specific autoantibodies. We also explore current therapeutic strategies, including commonly used broad-spectrum anti-inflammatory drugs, recent molecular-targeted therapies (e.g., Janus kinase inhibitors, monoclonal antibodies), and emerging cellular therapies such as chimeric antigen receptor T cells therapy and regulatory T-cell adoptive transfer. Incorporating knowledge from preclinical and clinical studies, this review synthesizes relevant information to inform about autoimmune diseases, bridge the gap from lab to clinic, and promote future advances through exploring precision medicine applications to meet clinical needs.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300212","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}
MedCommPub Date : 2025-06-16DOI: 10.1002/mco2.70190
Lan Mi, Jili Deng, Jiayue Qin, Chen Zhang, Lixia Liu, Shunli Yang, Libin Chen, Hua-Jun Wu, Haojie Wang, Jun Zhu, Hong Chen, Feng Lou, Shanbo Cao, Yuqin Song, Weiping Liu
{"title":"Genetic Subtype-Based International Prognostic Index Prognostic Model in Diffuse Large B-Cell Lymphoma","authors":"Lan Mi, Jili Deng, Jiayue Qin, Chen Zhang, Lixia Liu, Shunli Yang, Libin Chen, Hua-Jun Wu, Haojie Wang, Jun Zhu, Hong Chen, Feng Lou, Shanbo Cao, Yuqin Song, Weiping Liu","doi":"10.1002/mco2.70190","DOIUrl":"https://doi.org/10.1002/mco2.70190","url":null,"abstract":"<p>Molecular subtyping in diffuse large B-cell lymphoma (DLBCL) leads to facilitating drug selection. However, an integrated prognostic model based on molecular subtyping and clinical features has not been well established. Here, we retrospectively performed whole genome sequencing, whole exome sequencing, and fluorescence in situ hybridization in newly diagnosed DLBCLs, established a simplified LymphType algorithm for classification evaluation, and proposed a new integrated prognostic stratification system, combined molecular subtypes and International Prognostic Index (IPI) scoring system in our in-house sequencing cohort (<i>N</i> = 100), and validated in three public cohorts (<i>N</i> = 1480). Compared with IPI scoring system and classification algorithm model alone, the discrimination ability of prognostic model based on the new integrated model showed best discrimination of overall survival with concordance index value (0.773 vs. 0.724 vs. 0.648). We subsequently established a four-category risk model defined for the integrated prognostic model as follows: low, low-intermediate, high-intermediate, and high risk, demonstrating stronger prognostic separation across all end points (all <i>p </i>< 0.001) in our in-house cohort and three validation cohorts. Collectively, the new feasible integrated prognostic stratification system contributes to accurate prognosis assessment in clinical routine and provides a new basis for the follow-up treatment.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144300214","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}
MedCommPub Date : 2025-06-15DOI: 10.1002/mco2.70264
Jiayu Han, Jie Zhang, Yicheng Chen
{"title":"Key Roles in the Process of Extravasation and Colonization: Acyl-coenzyme A Synthetase Long-chain Family Member 4 and Polyunsaturated Lipids","authors":"Jiayu Han, Jie Zhang, Yicheng Chen","doi":"10.1002/mco2.70264","DOIUrl":"https://doi.org/10.1002/mco2.70264","url":null,"abstract":"<p>In a recent study published in <i>Cell</i>, Yilong Zou et al. [<span>1</span>] revealed dual functions of polyunsaturated fatty acyl (PUFA)-lipid in metastatic cancer cells. Acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL4), a PUFA-lipid biosynthesis enzyme, promotes hematogenous metastasis by enhancing membrane fluidity and cell invasiveness. Concurrently, elevated levels of PUFA-lipid induce reliance of cancer cells on enoyl-CoA delta isomerase 1 (ECI1) and enoyl-CoA hydratase 1 (ECH1), enzymes preparing UFAs for β-oxidation. Dual inhibition of ACSL4/ECH1 effectively suppresses tumor metastasis.</p><p>The majority of cancer patients succumb to metastatic disease rather than primary tumor burden [<span>2</span>]. Moreover, metastatic cancers remain largely incurable in clinical settings, ultimately leading to death due to systemic organ failure [<span>2</span>]. Extravasation, dormancy, and colonization are three major steps of metastasis [<span>2</span>] alongside other critical processes such as epithelial-to-mesenchymal transition. Factors impacting extravasation include increased cell motility and altered lipid phase behavior. At the same juncture, the metabolism of fatty acid and acyl-CoA plays an extremely significant role in the progression of cancer cell growth and metastasis [<span>3</span>].</p><p>Yilong Zou et al. conducted an analysis utilizing the Cancer Metastasis Map and the Cancer Therapeutics Response Portal to find whether metastatic cancer cells are more sensitive to specific cytotoxic compounds within the cancer cell lines listed in the dataset. These well-established databases serve as invaluable resources for oncology research, offering comprehensive datasets and insights that are worthy of further exploration. The results demonstrated that ovarian cancer cells exhibiting higher metastatic potential displayed increased sensitivity to ferroptosis induction. Subsequently, they utilized clinically collected metastatic samples to validate that ovarian cancer cells with higher metastatic potential showed increased susceptibility to ferroptosis and elevated levels of unsaturated lipids. Notably, emerging evidence indicates that oncogenic driver mutations may simultaneously prime cancer cells for ferroptosis vulnerability in breast and gastric adenocarcinomas [<span>4</span>].</p><p>To investigate the function of PUFA-lipids and ferroptosis-sensitizing factors in metastatic progression, an ovarian cancer metastasis model was established through intraperitoneal injection of GFP-firefly-luciferase-labeled ES-2 cells, a clear-cell carcinoma line derived from malignant ascites of ovarian cancer patients. Utilizing lipidomic analysis, the researchers found that PUFA-lipids increased in pulmonary metastatic lesions, without a corresponding change in the abundance of lipid droplets. This suggested a potential relationship between ferroptosis susceptibility and increased PUFA-lipids. To further minimize variability in","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292575","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 Interplay of Cross-Organ Immune Regulation in Inflammation and Cancer","authors":"Jie Dou, Jinzuo Jiang, Yangtao Xue, Xiaoqi Jiang, Yongzhuo Jiang, Peng Xiao, Junjie Xu","doi":"10.1002/mco2.70249","DOIUrl":"https://doi.org/10.1002/mco2.70249","url":null,"abstract":"<p>Organs dynamically interact with each other through immunomodulation to create a systemic immune response and influence disease progression. While traditional studies have tended to focus on single-organ immunity, recent studies have placed greater emphasis on reciprocal immune interactions between organs, such as those between the gut, liver, and brain. However, the precise mechanisms underlying these interorgan immune interactions remain unclear. Here, we synthesize the molecular and cellular bases of cross-organ immune regulation in the context of inflammation and neoplasia. Specifically, we describe the immune coordination between the gut, liver, and brain and how they immunomodulate other organs (including the thyroid, lung, cardiovascular system, kidney, bone, and skin). In addition, we explore clinical therapies that target these cross-organ immune modulations, the limitations of the treatments, and the potential benefits for patients. We also conclude by highlighting innovative technologies such as multiomics analysis, machine learning, and organ-on-a-chip platforms, which are providing unprecedented insights into interorgan immunity. Elucidating these mechanisms will advance precision medicine and enable the development of targeted therapies for diseases caused by cross-organ immunity.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70249","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292577","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}
MedCommPub Date : 2025-06-15DOI: 10.1002/mco2.70239
Junyi Wang, Lei Zhang, Yingying Liu, Yao Liu, Anying Xiong, Qin Ran, Xiang He, Vincent Kam Wai Wong, Colin Combs, Guoping Li, Min Wu
{"title":"Epithelial Atg5 Deficiency Intensifies Caspase-11 Activation, Fueling Extracellular mtDNA Release to Activate cGAS–STING–NLRP3 Axis in Macrophages During Pseudomonas Infection","authors":"Junyi Wang, Lei Zhang, Yingying Liu, Yao Liu, Anying Xiong, Qin Ran, Xiang He, Vincent Kam Wai Wong, Colin Combs, Guoping Li, Min Wu","doi":"10.1002/mco2.70239","DOIUrl":"https://doi.org/10.1002/mco2.70239","url":null,"abstract":"<p><i>Pseudomonas aeruginosa</i> (<i>P. aeruginosa</i>) infections pose a significant threat to public health, underscoring the need for deeper insights into host cellular defenses. This study explores the critical role of autophagy-related protein 5 (ATG5) in lung epithelial cells during <i>P. aeruginosa</i> infection. Single-cell RNA transcriptomics revealed a pronounced enrichment of autophagy pathways in type II alveolar epithelial cells (AEC2). Using a conditional <i>Atg5</i> knockout murine model, we demonstrated that ATG5 deficiency in AEC2 compromises survival, hampers bacterial clearance, and increases pathogen dissemination. Additionally, the loss of ATG5 exacerbated inflammatory responses, notably through the activation of the AKT/PI3K/NF-κB axis and pyroptosis, which culminated in severe lung injury and epithelial barrier disruption. Mechanistically, the absence of ATG5 disrupted mitophagy, leading to intensified mitochondrial damage. This exacerbated condition coupled with the activation of gasdermin D (GSDMD) by the noncanonical caspase-11, enhancing the release of mitochondrial DNA (mtDNA), which in turn activated cGAS–STING–NLRP3 signaling in macrophages. These findings highlight the essential role of ATG5 in modulating immune responses and suggest potential therapeutic targets for managing <i>P. aeruginosa</i>-induced pulmonary infections.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70239","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292574","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}
MedCommPub Date : 2025-06-15DOI: 10.1002/mco2.70203
Sofia Salta, José Pedro Sequeira, Bárbara Amorim-Fernandes, João Lobo, Inês Baldaque, Paula Monteiro, Fernando Tavares, Valérie Taly, Rui Henrique, Carmen Jerónimo
{"title":"Methylation-Specific Droplet Digital PCR: Testing a Novel Triage Tool for HrHPV-Positive Women in the Cervical Cancer Screening Program of Northern Portugal","authors":"Sofia Salta, José Pedro Sequeira, Bárbara Amorim-Fernandes, João Lobo, Inês Baldaque, Paula Monteiro, Fernando Tavares, Valérie Taly, Rui Henrique, Carmen Jerónimo","doi":"10.1002/mco2.70203","DOIUrl":"https://doi.org/10.1002/mco2.70203","url":null,"abstract":"<p>Dear Editor,</p><p>Cervical cancer remains a major global health problem. The most recent European guidelines endorsed HrHPV testing as the most cost-effective primary method for cervical cancer screening, with cytology being proposed as a triage test [<span>1</span>]. Although highly sensitive, this strategy depicts limited positive predictive value (PPV) [<span>1</span>], entailing increased referral to colposcopy units [<span>1</span>], ultimately leading to overdiagnosis and overtreatment. Indeed, we found that, in the Northern Region of Portugal, using cytology combined with HPV16/18 genotyping as triage for HrHPV-positive women, a fraction of those sent to the cervical pathology unit did not benefit from it [<span>2</span>]. Thus, alternative triage methods, such as dual p16/Ki67 staining (also known as CINtec PLUS) and DNA methylation markers, have emerged [<span>3, 4</span>]. Previously, we investigated the potential of methylation biomarkers for cervical cancer screening in the Portuguese population [<span>5</span>] and found that <i>MAL, FAM19A4</i>, and <i>hsa-miR124-2</i> promoter methylation levels were significantly higher in high-grade intraepithelial (HSIL) or worse (HSIL+) lesions in both compared tissue and cervical scrape samples [<span>5</span>]. However, some technical limitations became apparent, including the need for preamplification steps for the analysis of cervical scrapes [<span>5</span>]. More sensitive technologies for methylation assessment, such as droplet digital PCR (ddPCR), are required to overcome this limitation. Thus, we sought to develop a droplet digital methylation-specific PCR (ddMSP)-based assay to be used as a triage tool for referral to colposcopy among HrHPV-positive women in a well-established population-based cervical cancer screening program.</p><p>For this study, two patient cohorts (exploratory and replication) were selected. Relevant clinical data is depicted in Table S1. Leftovers from cervical scrapes primarily used for routine testing of women enrolled in the Regional Cervical Cancer Screening Program of Northern Portugal (RCCU-NP) were selected for this project. Further information may be found in Supporting Information.</p><p>For the exploratory series, 62 samples were selected from a previously characterized cohort of patients who tested positive for HrHPV and were referred to colposcopy between March and May 2019 [<span>5</span>]. For the replication series, all samples received in January 2020 that tested positive for HrHPV were considered eligible, except those without clinical information or enough DNA stored, which were excluded from analysis. DNA from all cervical scrapes collected was bisulfite treated and used for ddMSP assessment of <i>MAL</i> and <i>hsa-miR124-2</i> methylation levels (see protocols’ details in Supporting Information). Biomarker performance was assessed and compared to the current strategy applied in the RCCU-NP.</p><p>For the exploratory cohort, <i>MAL</i> an","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 7","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70203","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292578","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}
MedCommPub Date : 2025-06-11DOI: 10.1002/mco2.70253
Xinglu Miao, Pei Jiang, Zhaoping Wang, Weihua Kong, Lei Feng
{"title":"Mitochondrial Transplantation: A Novel Therapeutic Approach for Treating Diseases","authors":"Xinglu Miao, Pei Jiang, Zhaoping Wang, Weihua Kong, Lei Feng","doi":"10.1002/mco2.70253","DOIUrl":"https://doi.org/10.1002/mco2.70253","url":null,"abstract":"<p>Advances in mitochondrial biology have led to the development of mitochondrial transplantation as a novel and promising therapeutic strategy. This review provides a comprehensive analysis of the multifaceted roles of mitochondria in health and disease, highlighting their central functions in energy production, antioxidant defense, calcium signaling, apoptosis regulation, and mitochondrial homeostasis maintenance. We explore the mechanisms by which transplanted mitochondria exert their therapeutic effects, including restoring ATP production, attenuating oxidative stress, modulating inflammatory responses, reducing cellular apoptosis, promoting cell repair and regeneration, facilitating neural circuit reconstruction, and exhibiting antitumor properties. Key preclinical studies demonstrating the efficacy of mitochondrial transplantation across in vitro and in vivo disease models are discussed, along with the status of clinical trials. The review also critically compares mitochondrial transplantation with other mitochondria-targeted therapies, evaluating their relative advantages and limitations. Finally, we discuss the current challenges of translating this innovative therapy into clinical practice, such as mitochondrial isolation and purification, storage, targeted delivery, potential immune responses, and long-term safety and efficacy concerns. This review aims to stimulate further research and development in this promising field, paving the way for novel therapeutic interventions for various diseases.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70253","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256174","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}
MedCommPub Date : 2025-06-11DOI: 10.1002/mco2.70236
Qianqian Chen, Ming-Hua Zheng, Li Zhu, Fajuan Rui, Wenjing Ni, Yali Xiong, Xinyu Hu, Rahma Issa, Yixuan Zhu, Leyao Jia, Scott Barnett, Shengxia Yin, Chuanwu Zhu, Chao Wu, Mindie H. Nguyen, Jie Li
{"title":"Superior Diagnostic Efficacy of N-Terminal Propeptide of Type III Collagen and Golgi Protein 73 for Detection of Fibrosis in Chronic Hepatitis B Patients","authors":"Qianqian Chen, Ming-Hua Zheng, Li Zhu, Fajuan Rui, Wenjing Ni, Yali Xiong, Xinyu Hu, Rahma Issa, Yixuan Zhu, Leyao Jia, Scott Barnett, Shengxia Yin, Chuanwu Zhu, Chao Wu, Mindie H. Nguyen, Jie Li","doi":"10.1002/mco2.70236","DOIUrl":"https://doi.org/10.1002/mco2.70236","url":null,"abstract":"<p>Significant liver fibrosis is an indication for antiviral therapy in chronic hepatitis B (CHB). Using liver histology assessed by Scheuer system, we evaluated the diagnostic performance of PRO-C3, GP73, and their combination for the presence of liver fibrosis, and compared them with FIB-4, APRI, Agile 3+, FAST, and LSM in treatment-naïve CHB patients from two centers. The study included 324 patients, of whom 167 had S2–4 (significant fibrosis) and 83 had S3–4 (advanced fibrosis). PRO-C3 levels were higher in those with S2–4 and S3–4 compared with S0–1 and S0–2 (both <i>p </i>< 0.001), with similar findings for GP73. PRO-C3 and GP73 were independently associated with S2–4 and S3–4 in multivariable analyses. The area under the curves (AUCs) of PRO-C3 for S2–4 and S3–4 were 0.81 and 0.80, respectively, and exceeded those of GP73 (0.75 and 0.73). The combination of PRO-C3 and GP73 also had significantly higher AUCs for both S2–4 (0.84 vs. 0.64) and S3–4 (0.80 vs. 0.65) as compared with FIB-4, with similar findings for APRI, GP73, LSM, FAST, and Agile 3+ for S2–4. In conclusion, PRO-C3 alone or in combination with GP73 is highly predictive for detecting significant liver fibrosis among CHB patients.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70236","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256172","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":"Resveratrol: Molecular Mechanisms, Health Benefits, and Potential Adverse Effects","authors":"Zhuo-qun Ren, Sheng-yuan Zheng, Zhengcheng Sun, Yan Luo, Yu-tong Wang, Ping Yi, Yu-sheng Li, Cheng Huang, Wen-feng Xiao","doi":"10.1002/mco2.70252","DOIUrl":"https://doi.org/10.1002/mco2.70252","url":null,"abstract":"<p>Resveratrol (RES), a naturally occurring polyphenolic compound, has garnered significant attention due to its diverse biological activities, which include anti-inflammatory, antioxidant, and antiaging properties. This review synthesizes current evidence concerning the molecular mechanisms, therapeutic efficacy, and safety profile of RES across a variety of pathologies, with an emphasis on the latest research conducted in recent years. Mechanistically, RES is known to modulate critical signaling pathways such as the activation of sirtuin 1. These actions collectively contribute to the attenuation of oxidative stress, regulation of apoptosis, and promotion of autophagy. Preclinical studies have demonstrated the potential of RES in the mitigation of degenerative musculoskeletal disorders, cardiovascular diseases, cancer progression, and neurological diseases. Given the low bioavailability of RES and the potential for adverse reactions in clinical applications, we summarize and discuss its safety profile while outlining future research directions. This review underscores the therapeutic versatility of RES while advocating for rigorous pharmacokinetic optimization, standardized dosing protocols, and large-scale randomized controlled trials to validate its efficacy and safety in human populations.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 6","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70252","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256173","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}