IF 10.7

MedComm Pub Date : 2025-09-21 DOI: 10.1002/mco2.70395

Xinyuan Zhao, Xu Chen, Zihao Zhou, Jiarong Zheng, Yunfan Lin, Yucheng Zheng, Rongwei Xu, Shen Hu, Li Cui

{"title":"Advancements and Challenges in Salivary Metabolomics for Early Detection and Monitoring of Systemic Diseases","authors":"Xinyuan Zhao, Xu Chen, Zihao Zhou, Jiarong Zheng, Yunfan Lin, Yucheng Zheng, Rongwei Xu, Shen Hu, Li Cui","doi":"10.1002/mco2.70395","DOIUrl":"https://doi.org/10.1002/mco2.70395","url":null,"abstract":"Salivary metabolomics is increasingly recognized as a powerful, noninvasive approach for studying human health and disease. Unlike blood or urine, saliva is easily accessible, minimally invasive, and suitable for repeated sampling. Advances in nuclear magnetic resonance, mass spectrometry, capillary electrophoresis, and bioinformatics have improved the sensitivity and reproducibility of salivary metabolite profiling, enabling its use across diverse systemic diseases such as cancer, cardiovascular disorders, diabetes, viral infections, autoimmune diseases, and neurodegenerative conditions. Despite this progress, clinical translation is limited by variability in sampling, lack of standardized protocols, and insufficient large-scale validation. This review synthesizes recent developments in human salivary metabolomics, emphasizing disease-specific biomarkers and key applications in systemic disease diagnosis and monitoring. We also examine methodological and biological factors that influence data reliability, including collection methods, storage conditions, circadian rhythms, age, and host–microbiome interactions. Furthermore, integration of multiomics strategies, machine learning, and clinical registry data is discussed as a means to enhance biomarker discovery and translational potential. By addressing these challenges, salivary metabolomics can evolve into a reliable platform for noninvasive diagnosis, longitudinal disease monitoring, and personalized medicine, providing a valuable complement to blood-based diagnostics in precision healthcare.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70395","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111233","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}

引用次数: 0

Different Contribution of Missense and Loss-of-Function Variants to the Genetic Structure of Familial and Sporadic Meniere Disease 错义和功能缺失变异对家族性和散发性梅尼埃病遗传结构的不同贡献

IF 10.7

MedComm Pub Date : 2025-09-21 DOI: 10.1002/mco2.70394

Alberto M. Parra-Perez, Alvaro Gallego-Martinez, Alba Escalera-Balsera, Paula Robles-Bolivar, Patricia Perez-Carpena, Jose A. Lopez-Escamez

{"title":"Different Contribution of Missense and Loss-of-Function Variants to the Genetic Structure of Familial and Sporadic Meniere Disease","authors":"Alberto M. Parra-Perez, Alvaro Gallego-Martinez, Alba Escalera-Balsera, Paula Robles-Bolivar, Patricia Perez-Carpena, Jose A. Lopez-Escamez","doi":"10.1002/mco2.70394","DOIUrl":"https://doi.org/10.1002/mco2.70394","url":null,"abstract":"Meniere disease (MD) is a chronic inner ear disorder with significant heritability. This study compares the burden of rare high- and moderate-impact coding variants in an MD cohort to determine whether genetic burden in sporadic MD (SMD) overlaps familial MD (FMD), potentially revealing hidden inheritance in SMD. Exome sequencing identified rare variants in unrelated FMD (N = 93) and SMD (N = 287) patients. Gene Burden Analysis (GBA) was performed, and candidate genes were prioritized using the number of variant carriers, inner-ear expression, and hearing/balance-related phenotypic annotations. FMD patients showed higher accumulation of missense and loss-of-function variants than SMD, especially in genes linked to auditory and vestibular function. GBA identified 269 enriched genes in SMD, with 31 annotated for inner ear phenotypes, while FMD had 432 with 51 pinpointed. Sporadic and FMD overlapped in 28.1% of enriched genes, with ADGRV1, MEGF8, and MYO7A most commonly shared. Auditory brainstem responses from knockout mouse models supported hearing loss of three novel MD candidate genes (NIN, CCDC88C, and ANKRD24), consistent with patient hearing profiles. In conclusion, SMD and FMD have a divergent genetic architecture. The enrichment of missense variants in stria vascularis and hair cell stereocilia genes supports distinct pathogenic mechanisms and a multiallelic-recessive inheritance pattern in MD.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70394","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111172","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}

引用次数: 0

Free Radicals in Health and Disease 健康与疾病中的自由基

IF 10.7

MedComm Pub Date : 2025-09-21 DOI: 10.1002/mco2.70396

Xiaofeng Dai, Zizheng Huang, Ruohan Lyu

{"title":"Free Radicals in Health and Disease","authors":"Xiaofeng Dai, Zizheng Huang, Ruohan Lyu","doi":"10.1002/mco2.70396","DOIUrl":"https://doi.org/10.1002/mco2.70396","url":null,"abstract":"Free radicals, molecules with unpaired electrons, are double-edged swords. While they may cause damages to cells and threaten human health, they play essential roles in cellular signaling toward mitochondrial and immune homeostasis. Overproduction or insufficient supply of free radicals can both lead to health concerns and disease syndromes by causing oxidative or reductive stress to cells. Current redox therapies frequently fail clinically due to imprecise dosing and targeting, causing therapeutic futility or paradoxical harm by disrupting redox homeostasis, necessitating integrated frameworks linking redox biology to precision interventions alongside therapeutic innovation. This review explores free radicals’ generation sources, characterizes mitochondrial oxidative phosphorylation and pathological hyperglycemia as pivotal endogenous sources, and proposes oxygen and transition metals as fundamental regulators. This paper synthesizes multidimensional molecular mechanisms and pathologies arising from redox dysregulation and establishes reductive stress as a critical pathogenesis driver alongside oxidative stress. This review discusses free radical approaches and proposes cold atmospheric plasma as a transformative redox-modulating technology capable of bridging therapeutic dichotomies through calibrated interventions. By integrating mechanistic insights with innovative methodologies, this work underscores the imperative to innovatively harness the dual nature of free radicals for precision health and disease management.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70396","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111238","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}

引用次数: 0

Gene Therapy Targeting Pkp2 Deficiency Attenuates Cardiac Fibrosis: Insights From Single-Cell Transcriptomics in Pkp2-Knockout Rats 针对Pkp2缺失的基因治疗可减轻心脏纤维化：来自Pkp2敲除大鼠单细胞转录组学的见解

IF 10.7

MedComm Pub Date : 2025-09-18 DOI: 10.1002/mco2.70392

Xinyue Ding, Hui Zhang, Xuan Zhao, Nengpin Yin, Shuo Han, Xiao Jin, Tingting Li, Lina Xing, Zhen Qi, Yanan Zhu, Xin Wang, Zongjun Liu

{"title":"Gene Therapy Targeting Pkp2 Deficiency Attenuates Cardiac Fibrosis: Insights From Single-Cell Transcriptomics in Pkp2-Knockout Rats","authors":"Xinyue Ding, Hui Zhang, Xuan Zhao, Nengpin Yin, Shuo Han, Xiao Jin, Tingting Li, Lina Xing, Zhen Qi, Yanan Zhu, Xin Wang, Zongjun Liu","doi":"10.1002/mco2.70392","DOIUrl":"https://doi.org/10.1002/mco2.70392","url":null,"abstract":"Heart failure (HF), characterized by maladaptive cardiac fibrosis and progressive functional deterioration, remains a therapeutic challenge. In this study, we established a cardiac organoid HF model derived from human-induced pluripotent stem cells (hiPSCs) and observed a significant downregulation of the desmosomal protein plakophilin-2 (PKP2) in this model. Reduced PKP2 expression was detected in both HF rat and mouse. Subsequent in vivo studies on Pkp2-knockout (Pkp2-KO) rats demonstrated that adeno-associated virus serotype 9 (AAV9)-mediated restoration of PKP2 not only restored cardiac PKP2 expression but also attenuated the progression of fibrosis. Administration of AAV9-PKP2 could also inhibit myocardial fibrosis and slow down disease progression in HF mouse. Single-cell RNA sequencing analysis in rats revealed enriched pathological profibrotic cardiac fibroblasts (CFs) in PKP2-deficient myocardium. Mechanistically, AAV9-PKP2 administration induced the phenotypic conversion of activated CFs into quiescent antifibrotic states. Integrated bioinformatics identified that protein tyrosine phosphatase receptor type C (Ptprc) was a pivotal regulator orchestrating this cellular reprogramming. Our findings thus unveil PKP2 as a master regulator of fibroblast activation and propose AAV9-PKP2 gene therapy as a promising novel therapeutic strategy targeting pathological fibrosis in HF.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70392","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102038","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}

引用次数: 0

Mitochondria-Associated Endoplasmic Reticulum Membranes in Health and Diseases 线粒体相关内质网膜在健康和疾病中的作用

IF 10.7

MedComm Pub Date : 2025-09-18 DOI: 10.1002/mco2.70379

Hangnan Hong, Zhenyang Guo, Junbo Ge, Hua Li

{"title":"Mitochondria-Associated Endoplasmic Reticulum Membranes in Health and Diseases","authors":"Hangnan Hong, Zhenyang Guo, Junbo Ge, Hua Li","doi":"10.1002/mco2.70379","DOIUrl":"https://doi.org/10.1002/mco2.70379","url":null,"abstract":"Membrane contact sites enable organelles to interact closely, thereby coordinating cellular homeostasis and functional regulation. Among diverse subcellular membrane architectures, mitochondria-associated endoplasmic reticulum membranes (MAMs) assume a crucial role in the physiological and pathological environments. A plethora of cellular processes are intertwined with MAMs, such as Ca2+ translocation, lipid metabolism, endoplasmic reticulum (ER) stress response, mitochondrial dynamics, and mitophagy. In the event of improper modulation of MAMs components, the incidence of diseases would surge remarkably. This review endeavors to expound upon the functions of key MAMs proteins in healthy state and decipher their regulatory mechanisms under physiological and pathological circumstances. In addition, we try to probe into the specific contribution of MAMs within the occurrence and development of diseases, and subsequently collate drug compounds and clinical trials that target MAMs components. Finally, we proffer our insights regarding the contentious perspectives and prospective research directions of MAMs. Understanding the roles and mechanisms of MAMs may potentially offer novel diagnostic biomarkers and treatment targets in clinical practice, paving the way for more precise and effective clinical interventions for common diseases.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102030","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}

引用次数: 0

Correction to “Depletion of Fat Mass and Obesity-Associated Protein (FTO) Drives Heterochromatin Loss via Lysine Acetyltransferase 8 (KAT8)-Mediated Remodeling and Spacing Factor 1 (RSF1) Acetylation in Skin Aging” 对“皮肤衰老中赖氨酸乙酰转移酶8 （KAT8）介导的重塑和间隔因子1 （RSF1）乙酰化介导的脂肪量和肥胖相关蛋白（FTO）消耗驱动异染色质损失”的修正

IF 10.7

MedComm Pub Date : 2025-09-18 DOI: 10.1002/mco2.70384

{"title":"Correction to “Depletion of Fat Mass and Obesity-Associated Protein (FTO) Drives Heterochromatin Loss via Lysine Acetyltransferase 8 (KAT8)-Mediated Remodeling and Spacing Factor 1 (RSF1) Acetylation in Skin Aging”","authors":"","doi":"10.1002/mco2.70384","DOIUrl":"https://doi.org/10.1002/mco2.70384","url":null,"abstract":"F. Wang, L. Zhou, Y. Zhong, et al., “Depletion of Fat Mass and Obesity-Associated Protein (FTO) Drives Heterochromatin Loss via Lysine Acetyltransferase 8 (KAT8)-Mediated Remodeling and Spacing Factor 1 (RSF1) Acetylation in Skin Aging,” MedComm 6, no. 7 (2025): e70205, https://doi.org/10.1002/mco2.70205.In the process of checking the raw data [1], the authors noticed an inadvertent mistake occurring in Figure 4C that needed to be corrected after the online publication of the article. The correct result should be as shown below. The authors apologize for these oversights and declare that this correction does not affect the description, interpretation, or conclusions detailed in the original manuscript.1. F. Wang, L. Zhou, Y. Zhong, et al. “Depletion of Fat Mass and Obesity-Associated Protein (FTO) Drives Heterochromatin Loss via Lysine Acetyltransferase 8 (KAT8)-Mediated Remodeling and Spacing Factor 1 (RSF1) Acetylation in Skin Aging,” MedComm 6, no. 7 (2025): e70205. https://doi.org/10.1002/mco2.70205.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70384","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102039","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}

引用次数: 0

Role of Neutrophils in Homeostasis and Diseases 中性粒细胞在体内平衡和疾病中的作用

IF 10.7

MedComm Pub Date : 2025-09-18 DOI: 10.1002/mco2.70390

Xingyu Chang, Yulin Liu, Junjun Qiu, Keqin Hua

{"title":"Role of Neutrophils in Homeostasis and Diseases","authors":"Xingyu Chang, Yulin Liu, Junjun Qiu, Keqin Hua","doi":"10.1002/mco2.70390","DOIUrl":"https://doi.org/10.1002/mco2.70390","url":null,"abstract":"Neutrophils, constituting a predominant subset of innate immune cells in mammalian systems, play pivotal roles in pathogenic clearance and homeostatic maintenance. In the progressive development of cancer, neutrophils exert dual roles in both anticancer and procancer processes through their heterogeneity. In recent years, research into the role of neutrophils in cancer and various nontumor diseases has been continuously deepening. However, current research in this area remains incomplete. This review comprehensively summarizes the tissue homing dynamics, lifespan regulation, and physiological functions of neutrophils, starting from their development and heterogeneity. Furthermore, we delineate the dual regulatory functions of neutrophils in carcinogenesis, encompassing both tumor-suppressive mechanisms and protumor mechanisms. This section further synthesizes recent advancements in neutrophil-targeted therapeutic platforms and biomimetic delivery systems, while critically evaluating persistent methodological and translational challenges in clinical applications. In addition, we systematically analyze the role of neutrophils in non-neoplastic diseases and list several typical diseases, including infectious diseases. Finally, we also discuss current controversies and research perspectives on neutrophils. It is hoped that this review will deepen insights into the role of neutrophils in homeostasis and disease, while exploring their potential in disease treatment.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70390","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102031","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}

引用次数: 0

G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers G蛋白偶联受体信号：癌症的意义和治疗进展。

IF 10.7

MedComm Pub Date : 2025-09-16 DOI: 10.1002/mco2.70375

Inamu Rashid Khan, Sana Khurshid, Saud Almawash, Rakesh Kumar, Ammira S. Al-Shabeeb Akil, Ajaz A. Bhat, Muzafar A. Macha

{"title":"G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers","authors":"Inamu Rashid Khan, Sana Khurshid, Saud Almawash, Rakesh Kumar, Ammira S. Al-Shabeeb Akil, Ajaz A. Bhat, Muzafar A. Macha","doi":"10.1002/mco2.70375","DOIUrl":"10.1002/mco2.70375","url":null,"abstract":"G protein-coupled receptors (GPCRs) are the largest and most diverse class of membrane proteins, mediating cellular responses to a wide range of extracellular stimuli. GPCRs initiate complex intracellular signaling networks that regulate vital physiological functions and are associated with numerous diseases, including various types of cancer. Their conserved seven-transmembrane (7TM) structure enables these signaling networks by allowing interactions with multiple ligands and intracellular effectors. In several types of tumors, abnormal GPCR signaling promotes carcinogenesis by supporting immune evasion, cell proliferation, and therapeutic resistance. A significant research gap exists in fully understanding the molecular mechanisms behind pathway-specific activation and biased ligand discovery of GPCRs, which could lead to the development of more effective therapies. This review examines the complexity of GPCRs, with a focus on their role in signaling through the differential activation of pathways regulated by β-arrestin and G proteins. It discusses how targeted modulation of signaling outcomes by receptor mutants might offer therapeutic benefits in cancer treatment. The review also highlights emerging technologies, such as aptamers, PROTACs, and nanobodies, that more precisely target GPCRs. In addition to exploring receptor structure–function relationships and pathway selectivity, this review provides valuable insights into GPCR-biased signaling and its implications in cancer biology.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145088689","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}

引用次数: 0

PACLseq: A Standalone Diagnostic Method for Ph-Like Acute Lymphoblastic Leukemia Using Nanopore Sequencing PACLseq：使用纳米孔测序的ph样急性淋巴细胞白血病的独立诊断方法。

IF 10.7

MedComm Pub Date : 2025-09-16 DOI: 10.1002/mco2.70360

Hang Zhang, Huan Yu, Yanmei Chen, Kai Jiang, Beibei Huo, Jialin Li, Ting Liu, Dan Xie

{"title":"PACLseq: A Standalone Diagnostic Method for Ph-Like Acute Lymphoblastic Leukemia Using Nanopore Sequencing","authors":"Hang Zhang, Huan Yu, Yanmei Chen, Kai Jiang, Beibei Huo, Jialin Li, Ting Liu, Dan Xie","doi":"10.1002/mco2.70360","DOIUrl":"10.1002/mco2.70360","url":null,"abstract":"Timely and accurate detection of Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL)-related fusion gene is essential for treatment decisions. However, due to the complexity of possible gene fusion combinations of Ph-like ALL, current diagnostic workflows face critical limitations: prolonged turnaround (7–14 days), high costs, and deficiency in degraded specimens. In this study, we introduce Partial Anchored Capture and Long-Read Sequencing (PACLseq), a nanopore-sequencing-technology-based approach. We designed a detection panel associated with Ph-like ALL, specifically ABL2, CSF1R, PDGFRB, JAK2, ABL1, EPOR, and CRLF2 as target genes. Validated on 47 clinical samples, PACLseq achieved 93.3% sensitivity and 100% specificity in 26 degraded RNA samples (RIN > 3). Crucially, PACLseq maintained detection accuracy in nine low-RIN samples (RIN ≤ 3) with fragmented transcripts. The method requires only 10 ng of RNA input, delivers results in 3 days (vs. 7–14 days for conventional methods), and reduces costs by 50%. By offering rapid and accurate fusion detection, PACLseq has the potential to significantly improve diagnostic efficiency, facilitate timely treatment decisions, and enhance patient outcomes in the management of Ph-like ALL.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145088706","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}

引用次数: 0

Keratinocyte Autophagy-Mediated Self-Assembling Tetrahedral Framework Nucleic Acid Induces Wound Healing and Reduces Scar Hyperplasia 角质细胞自噬介导的自组装四面体框架核酸诱导伤口愈合并减少疤痕增生。

IF 10.7

MedComm Pub Date : 2025-09-16 DOI: 10.1002/mco2.70355

Jian Jin, Jia-Jie Li, Zi-Han Tao, Rong-Jia Li, Zi-Liang Zhang, Qing-Song Liu, Zheng-Li Chen, Ji-Qiu Chen, Chen-Ru Wei, Lei Liu, Liang-Liang Zhu, Shi-Hui Zhu, Yun-Feng Lin

{"title":"Keratinocyte Autophagy-Mediated Self-Assembling Tetrahedral Framework Nucleic Acid Induces Wound Healing and Reduces Scar Hyperplasia","authors":"Jian Jin, Jia-Jie Li, Zi-Han Tao, Rong-Jia Li, Zi-Liang Zhang, Qing-Song Liu, Zheng-Li Chen, Ji-Qiu Chen, Chen-Ru Wei, Lei Liu, Liang-Liang Zhu, Shi-Hui Zhu, Yun-Feng Lin","doi":"10.1002/mco2.70355","DOIUrl":"10.1002/mco2.70355","url":null,"abstract":"Tetrahedral framework nucleic acid (tFNA) efficiently treats various diseases; however, its effect on wound healing is unknown. We investigated tFNA's impact on human immortalized epidermal cells (HaCaT) cells and wound healing through in vitro and in vivo experiments. The tFNA is taken up by cells and exhibits good biocompatibility. Transmission electron microscopy and autophagic flux assays showed that tFNA substantially increased the number of intracellular autophagosomes, thus suggesting the activation of cell autophagy. Immunofluorescence and western blotting results indicated decreased microtubule-associated protein 1 light chain 3I (LC 3I) and prostacyclin (P62) levels, and increased microtubule-associated protein 1 light chain 3II (LC 3II), suggesting increased autophagic activity. Adenosine 5′-monophosphate-activated protein kinase (AMPK) and unc-51-like kinase 1 (ULK1) activation, and mechanistic target of rapamycin (mTOR) inhibition were also observed, suggesting their involvement in tFNA-induced cell activation. Autophagy-related protein (ATG) 5 and ATG7 knockdown in HaCaT cells reverse confirmed these results. Animal experiment results mirrored the cellular findings, revealing autophagy induction, wound healing promotion, and effective scar score reduction. These results suggest that tFNA promotes HaCaT cell autophagy activation through mTOR pathway inhibition, promoting wound healing and reducing scarring. Our findings expand the application of tFNA and highlight new avenues for clinical wound treatment.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145088723","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}

引用次数: 0

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