{"title":"Reduced intestinal-to-diffuse conversion and immunosuppressive responses underlie superiority of neoadjuvant immunochemotherapy in gastric adenocarcinoma","authors":"Lei Wang, Linghong Wan, Xu Chen, Peng Gao, Yongying Hou, Linyu Wu, Wenkang Liu, Shuoran Tian, Mengyi Han, Shiyin Peng, Yuting Tan, Yuwei Pan, Yuanfeng Ren, Jinyang Li, Haihui Wen, Qin Liu, Mengsi Zhang, Tao Wang, Zhong-Yi Qin, Junyu Xiang, Dongfeng Chen, Xianfeng Li, Shu-Nan Wang, Chuan Chen, Mengxia Li, Fan Li, Zhenning Wang, Bin Wang","doi":"10.1002/mco2.762","DOIUrl":"https://doi.org/10.1002/mco2.762","url":null,"abstract":"<p>Neoadjuvant immunochemotherapy (NAIC) achieves superior clinical benefits over neoadjuvant chemotherapy (NAC) in multiple types of human cancers, including gastric adenocarcinoma (GAC). However, it is poorly understood how the malignant epithelial cells and tumor immune microenvironment (TIME) might respond distinctly to NAIC and NAC that underlies therapeutic efficacy. Here treatment-naive and paired tumor tissues from multiple centers were subjected to pathological, immunological, and transcriptomic analysis. NAIC demonstrated significantly increased rate of pathological complete response compared to NAC (pCR: 25% vs. 4%, <i>p </i>< 0.05). Interestingly, pretreatment intestinal subtype of Lauren's classification was predictive of pathologic regression following NAIC, but not NAC. A substantial portion of cancers underwent intestinal-to-diffuse transition, which occurred less following NAIC and correlated with treatment failure. Moreover, NAIC prevented reprogramming to an immunosuppressive TIME with less active fibroblasts and exhausted CD8<sup>+</sup> T cells, and increased numbers of mature tertiary lymphoid structures. Mechanistically, activation of the tumor necrosis factor alpha (TNFα)/nuclear factor-kappa B (NF-κB) signaling pathway was associated with response to NAIC. Together, NAIC is superior to NAC for locally advanced GAC, likely due to reduced intestinal-to-diffuse conversion and reprogramming to an immuno-active TIME. Modulation of the histological conversion and immunosuppressive TIME could be translatable approaches to improve neoadjuvant therapeutic efficacy.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.762","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142540962","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":"Comprehensive single-cell profiling of monocytes in HLA-B27-positive ankylosing spondylitis with acute anterior uveitis","authors":"Huan Li, Xueming Ju, Lixin Zhang, Jing Zhu, Jing Zhang, Jialing Xiao, Ting Wang, Weijia Wu, Liang Wang, Chengzi Gan, Xiangmei Li, Yutong Wei, Siyu Zhu, Yu Zhou, Bolin Deng, Ning Xiao, Bo Gong","doi":"10.1002/mco2.759","DOIUrl":"https://doi.org/10.1002/mco2.759","url":null,"abstract":"<p>Acute anterior uveitis (AAU) is a common extra-articular manifestation of ankylosing spondylitis (AS), particularly in patients positive for the human leucocyte antigen (HLA)-B27 genetic marker. To explore the underlying mechanisms of HLA-B27<sup>+</sup> AS-associated AAU, we employed single-cell RNA sequencing to profile the transcriptomes of peripheral blood mononuclear cells in three HLA-B27<sup>+</sup> AS-associated AAU patients and three healthy controls (HCs). We identified 11 distinct immune cell clusters, with a particular focus on monocytes, revealing six subsets, including three previously unidentified subsets, namely, GTPase immune-associated proteins, Th17-related, and lncRNA monocytes, with unique gene expression patterns. Significant differences in monocyte composition, activation states, and gene expression were observed between patients and HCs, particularly within HLA monocyte subpopulations. Notably, enhanced expression of X-inactive specific transcript and myeloid cell nuclear differentiation antigen genes was validated across monocyte subclusters in patients. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis highlighted significant enrichment in antigen processing and presentation pathways, shedding light on the disease's molecular mechanisms. These findings provide novel insights into the molecular mechanisms of HLA-B27<sup>+</sup> AS-associated AAU and may contribute to the development of targeted diagnostic and therapeutic strategies. Further clinical validation is essential.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.759","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142540961","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 immunosenescence for improved tumor immunotherapy","authors":"Zaoqu Liu, Lulu Zuo, Zhaokai Zhou, Shutong Liu, Yuhao Ba, Anning Zuo, Yuqing Ren, Chuhan Zhang, Yukang Chen, Hongxuan Ma, Yudi Xu, Peng Luo, Quan Cheng, Hui Xu, Yuyuan Zhang, Siyuan Weng, Xinwei Han","doi":"10.1002/mco2.777","DOIUrl":"https://doi.org/10.1002/mco2.777","url":null,"abstract":"<p>Tumor immunotherapy has significantly transformed the field of oncology over the past decade. An optimal tumor immunotherapy would ideally elicit robust innate and adaptive immune responses within tumor immune microenvironment (TIME). Unfortunately, immune system experiences functional decline with chronological age, a process termed “immunosenescence,” which contributes to impaired immune responses against pathogens, suboptimal vaccination outcomes, and heightened vulnerability to various diseases, including cancer. In this context, we will elucidate hallmarks and molecular mechanisms underlying immunosenescence, detailing alterations in immunosenescence at molecular, cellular, organ, and disease levels. The role of immunosenescence in tumorigenesis and senescence-related extracellular matrix (ECM) has also been addressed. Recognizing that immunosenescence is a dynamic process influenced by various factors, we will evaluate treatment strategies targeting hallmarks and molecular mechanisms, as well as methods for immune cell, organ restoration, and present emerging approaches in immunosenescence for tumor immunotherapy. The overarching goal of immunosenescence research is to prevent tumor development, recurrence, and metastasis, ultimately improving patient prognosis. Our review aims to reveal latest advancements and prospective directions in the field of immunosenescence research, offering a theoretical basis for development of practical anti-immunosenescence and anti-tumor strategies.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.777","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142540977","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}
Ming-Ge Shi, Xin-Meng Feng, Hao-Yang Zhi, Lei Hou, Dong-Fu Feng
{"title":"Machine learning-based radiomics in neurodegenerative and cerebrovascular disease","authors":"Ming-Ge Shi, Xin-Meng Feng, Hao-Yang Zhi, Lei Hou, Dong-Fu Feng","doi":"10.1002/mco2.778","DOIUrl":"https://doi.org/10.1002/mco2.778","url":null,"abstract":"<p>Cognitive impairments, which can be caused by neurodegenerative and cerebrovascular disease, represent a growing global health crisis with far-reaching implications for individuals, families, healthcare systems, and economies worldwide. Notably, neurodegenerative-induced cognitive impairment often presents a different pattern and severity compared to cerebrovascular-induced cognitive impairment. With the development of computational technology, machine learning techniques have developed rapidly, which offers a powerful tool in radiomic analysis, allowing a more comprehensive model that can handle high-dimensional, multivariate data compared to the traditional approach. Such models allow the prediction of the disease development, as well as accurately classify disease from overlapping symptoms, therefore facilitating clinical decision making. This review will focus on the application of machine learning-based radiomics on cognitive impairment caused by neurogenerative and cerebrovascular disease. Within the neurodegenerative category, this review primarily focuses on Alzheimer's disease, while also covering other conditions such as Parkinson's disease, Lewy body dementia, and Huntington's disease. In the cerebrovascular category, we concentrate on poststroke cognitive impairment, including ischemic and hemorrhagic stroke, with additional attention given to small vessel disease and moyamoya disease. We also review the specific challenges and limitations when applying machine learning radiomics, and provide our suggestion to overcome those limitations towards the end, and discuss what could be done for future clinical use.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.778","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142540978","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":"Cardiomyopathy: pathogenesis and therapeutic interventions","authors":"Shitong Huang, Jiaxin Li, Qiuying Li, Qiuyu Wang, Xianwu Zhou, Jimei Chen, Xuanhui Chen, Abdelouahab Bellou, Jian Zhuang, Liming Lei","doi":"10.1002/mco2.772","DOIUrl":"10.1002/mco2.772","url":null,"abstract":"<p>Cardiomyopathy is a group of disease characterized by structural and functional damage to the myocardium. The etiologies of cardiomyopathies are diverse, spanning from genetic mutations impacting fundamental myocardial functions to systemic disorders that result in widespread cardiac damage. Many specific gene mutations cause primary cardiomyopathy. Environmental factors and metabolic disorders may also lead to the occurrence of cardiomyopathy. This review provides an in-depth analysis of the current understanding of the pathogenesis of various cardiomyopathies, highlighting the molecular and cellular mechanisms that contribute to their development and progression. The current therapeutic interventions for cardiomyopathies range from pharmacological interventions to mechanical support and heart transplantation. Gene therapy and cell therapy, propelled by ongoing advancements in overarching strategies and methodologies, has also emerged as a pivotal clinical intervention for a variety of diseases. The increasing number of causal gene of cardiomyopathies have been identified in recent studies. Therefore, gene therapy targeting causal genes holds promise in offering therapeutic advantages to individuals diagnosed with cardiomyopathies. Acting as a more precise approach to gene therapy, they are gradually emerging as a substitute for traditional gene therapy. This article reviews pathogenesis and therapeutic interventions for different cardiomyopathies.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515517","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":"Metabolic regulation of intestinal homeostasis: molecular and cellular mechanisms and diseases","authors":"Ruolan Zhang, Ansu Perekatt, Lei Chen","doi":"10.1002/mco2.776","DOIUrl":"10.1002/mco2.776","url":null,"abstract":"<p>Metabolism serves not only as the organism's energy source but also yields metabolites crucial for maintaining tissue homeostasis and overall health. Intestinal stem cells (ISCs) maintain intestinal homeostasis through continuous self-renewal and differentiation divisions. The intricate relationship between metabolic pathways and intestinal homeostasis underscores their crucial interplay. Metabolic pathways have been shown to directly regulate ISC self-renewal and influence ISC fate decisions under homeostatic conditions, but the cellular and molecular mechanisms remain incompletely understood. Understanding the intricate involvement of various pathways in maintaining intestinal homeostasis holds promise for devising innovative strategies to address intestinal diseases. Here, we provide a comprehensive review of recent advances in the regulation of intestinal homeostasis. We describe the regulation of intestinal homeostasis from multiple perspectives, including the regulation of intestinal epithelial cells, the regulation of the tissue microenvironment, and the key role of nutrient metabolism. We highlight the regulation of intestinal homeostasis and ISC by nutrient metabolism. This review provides a multifaceted perspective on how intestinal homeostasis is regulated and provides ideas for intestinal diseases and repair of intestinal damage.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515519","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":"Partial reduction of interleukin-33 signaling improves senescence and renal injury in diabetic nephropathy","authors":"Li Chen, Chao Gao, Xingzhu Yin, Li Mo, Xueer Cheng, Huimin Chen, Chunjie Jiang, Bangfu Wu, Ying Zhao, Hongxia Li, Yanyan Li, Jiansha Li, Liangkai Chen, Qianchun Deng, Ping Yao, Yuhan Tang","doi":"10.1002/mco2.742","DOIUrl":"10.1002/mco2.742","url":null,"abstract":"<p>Diabetic nephropathy (DN) is a frequent and costly complication of diabetes with limited understandings of mechanisms and therapies. Emerging evidence points to the important roles of interleukin-33 (IL-33) in acute kidney injury, yet its contribution to DN is still unclear. We here found a ubiquitous increase of IL-33 and its receptor (ST2) in murine models and patients with DN. Surprisingly, both IL-33 and ST2 knockdown aggravated renal lesions in DN, while overexpression of IL-33 also exacerbated the condition. Further population-based analyses revealed a positive correlation of IL-33 expression with renal dysfunction in DN patients. Individuals with high IL-33 expression-related polygenic risk score had a higher DN risk. These findings confirmed the harmful effects of IL-33 on DN. Conversely, endogenous and exogenous partial reduction of IL-33 signaling conferred renoprotective effects in vivo and in vitro. Mechanistically, IL-33 induced senescence by regulating cell cycle factors in HK-2 cells, and accordingly senescence led to renal cell damage through the secretion of senescence-related secretory phenotype (SASP) including IL-33 and prostaglandins. Together, elevated IL-33 accelerates cellular senescence to drive DN possibly by SASP production, while a partial blockage improves renal injury and senescence. Our findings pinpoint a possible and new avenue for DN interventions.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515520","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":"Robust tetra-armed poly (ethylene glycol)-based hydrogel as tissue bioadhesive for the efficient repair of meniscus tears","authors":"Jing Ye, Yourong Chen, Ronghui Deng, Jiying Zhang, Hufei Wang, Shitang Song, Xinjie Wang, Bingbing Xu, Xing Wang, Jia-Kuo Yu","doi":"10.1002/mco2.738","DOIUrl":"10.1002/mco2.738","url":null,"abstract":"<p>Repair and preservation of the injured meniscus has become paramount in clinical practice. However, the complexities of various clinic stitching techniques for meniscus repair pose challenges for grassroots doctors. Hence, there is a compelling interest in innovative therapeutic strategies such as bioadhesives. An ideal bioadhesive must cure quickly in aqueous and blood environments, bind strongly, endure arthroscopic washing pressures, and degrade appropriately for tissue regeneration. Here, we present a tetra-poly (ethylene glycol) (PEG)-based hydrogel bioadhesive, boasting high biocompatibility, ultrafast gelation, facile injectable operation, and favorable mechanical strength. In view of the synergistic effects of chemical anchor and physical chain entanglement to tightly bind the meniscus, a seamless interface was formed between the surrounding meniscal tissues and hydrogels, enabling the longitudinal tear of the meniscus fused in situ to withstand large tensile force with the adhesive strength of 541.5 ± 31.4 kPa and arthroscopic washout resistance of 29.4 kPa. Superior to existing commercial adhesives, ours allows sutureless application and arthroscopic assistance, without requiring specialized clinical skills. This research is expected to significantly impact our understanding of meniscal healing and ultimately promote a simpler process for achieving functional and structural recovery in torn menisci.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515523","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}
Tobias Woehrle, Florian Pfeiffer, Maximilian M. Mandl, Wolfgang Sobtzick, Jörg Heitzer, Alisa Krstova, Luzie Kamm, Matthias Feuerecker, Dominique Moser, Matthias Klein, Benedikt Aulinger, Michael Dolch, Anne-Laure Boulesteix, Daniel Lanz, Alexander Choukér
{"title":"Point-of-care breath sample analysis by semiconductor-based E-Nose technology discriminates non-infected subjects from SARS-CoV-2 pneumonia patients: a multi-analyst experiment","authors":"Tobias Woehrle, Florian Pfeiffer, Maximilian M. Mandl, Wolfgang Sobtzick, Jörg Heitzer, Alisa Krstova, Luzie Kamm, Matthias Feuerecker, Dominique Moser, Matthias Klein, Benedikt Aulinger, Michael Dolch, Anne-Laure Boulesteix, Daniel Lanz, Alexander Choukér","doi":"10.1002/mco2.726","DOIUrl":"10.1002/mco2.726","url":null,"abstract":"<p>Metal oxide sensor-based electronic nose (E-Nose) technology provides an easy to use method for breath analysis by detection of volatile organic compound (VOC)-induced changes of electrical conductivity. Resulting signal patterns are then analyzed by machine learning (ML) algorithms. This study aimed to establish breath analysis by E-Nose technology as a diagnostic tool for severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) pneumonia within a multi-analyst experiment. Breath samples of 126 subjects with (<i>n</i> = 63) or without SARS-CoV-2 pneumonia (<i>n</i> = 63) were collected using the ReCIVA® Breath Sampler, enriched and stored on Tenax sorption tubes, and analyzed using an E-Nose unit with 10 sensors. ML approaches were applied by three independent data analyst teams and included a wide range of classifiers, hyperparameters, training modes, and subsets of training data. Within the multi-analyst experiment, all teams successfully classified individuals as infected or uninfected with an averaged area under the curve (AUC) larger than 90% and misclassification error lower than 19%, and identified the same sensor as most relevant to classification success. This new method using VOC enrichment and E-Nose analysis combined with ML can yield results similar to polymerase chain reaction (PCR) detection and superior to point-of-care (POC) antigen testing. Reducing the sensor set to the most relevant sensor may prove interesting for developing targeted POC testing.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515521","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 dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions","authors":"Honghong Jiang, Yiming Guo, Qihang Wang, Yiran Wang, Dingchuan Peng, Yigong Fang, Lei Yan, Zhuolin Ruan, Sheng Zhang, Yong Zhao, Wendan Zhang, Wei Shang, Zhichun Feng","doi":"10.1002/mco2.785","DOIUrl":"10.1002/mco2.785","url":null,"abstract":"<p>The complement system, comprising over 30 proteins, is integral to the immune system, and the coagulation system is critical for vascular homeostasis. The activation of the complement and coagulation systems involves an organized proteolytic cascade, and the overactivation of these systems is a central pathogenic mechanism in several diseases. This review describes the role of complement and coagulation system activation in critical illness, particularly sepsis. The complexities of sepsis reveal significant knowledge gaps that can be compared to a profound abyss, highlighting the urgent need for further investigation and exploration. It is well recognized that the inflammatory network, coagulation, and complement systems are integral mechanisms through which multiple factors contribute to increased susceptibility to infection and may result in a disordered immune response during septic events in patients. Given the overlapping pathogenic mechanisms in sepsis, immunomodulatory therapies currently under development may be particularly beneficial for patients with sepsis who have concurrent infections. Herein, we present recent findings regarding the molecular relationships between the coagulation and complement pathways in the advancement of sepsis, and propose potential intervention targets related to the crosstalk between coagulation and complement, aiming to provide more valuable treatment of sepsis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515524","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}