JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献_第3页

Gas Plasma Exposure Attenuates the Inflammatory Rheumatoid Arthritis-Like Phenotype of Murine Synoviocytes in Vitro 体外小鼠滑膜细胞炎性类风湿关节炎样表型研究

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-26 DOI: 10.1111/jcmm.71118

Marcel Kordt, Wendy Bergmann-Ewert, Johann Aleith, Sander Bekeschus, Brigitte Müller-Hilke

{"title":"Gas Plasma Exposure Attenuates the Inflammatory Rheumatoid Arthritis-Like Phenotype of Murine Synoviocytes in Vitro","authors":"Marcel Kordt, Wendy Bergmann-Ewert, Johann Aleith, Sander Bekeschus, Brigitte Müller-Hilke","doi":"10.1111/jcmm.71118","DOIUrl":"10.1111/jcmm.71118","url":null,"abstract":"Rheumatoid arthritis (RA) is driven by hyperplastic fibroblast-like synoviocytes (FLS) that adopt a persistent inflammatory and invasive phenotype, often resistant to conventional therapies. Here, we investigated whether cold gas plasma exposure modulates inflammatory FLS (iFLS) in vitro. Primary murine FLS were primed with TNF-α to induce an inflammatory phenotype and exposed to an argon plasma jet for 30–150 s; argon gas alone served as a control. Gas plasma treatment caused a rapid, dose-dependent rise in intracellular reactive oxygen species and free thiols, followed by partial resolution by 24 h. This oxidative burst coincided with mitochondrial dysfunction and progressive loss of cell viability. Surviving iFLS exhibited markedly reduced inflammatory features, such as surface levels of ICAM-1 (CD54), VCAM-1 (CD106), and Thy-1 (CD90.2), along with diminished production of IL-6 and CCL2 at higher doses. Reflecting the impaired expression of inflammation-associated adhesion molecules. Furthermore, plasma treatment significantly delayed iFLS migration. Together, these findings suggest that cold gas plasma has cytotoxic effects on a subset of iFLS induced by acute oxidative stress, as well as reprogramming surviving iFLS towards a less aggressive phenotype. These in vitro data establish a foundation for further research in synovial explants and arthritis models, as well as for systematic safety testing in non-inflammatory joint-resident cells.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521078","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

ALDH2 Mediated Ferroptosis Regulation in Ischemia–Reperfusion Injury 缺血-再灌注损伤中ALDH2介导的铁下垂调节。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-25 DOI: 10.1111/jcmm.71072

Liang Han, Wen Zhai

{"title":"ALDH2 Mediated Ferroptosis Regulation in Ischemia–Reperfusion Injury","authors":"Liang Han, Wen Zhai","doi":"10.1111/jcmm.71072","DOIUrl":"10.1111/jcmm.71072","url":null,"abstract":"Ischemia–reperfusion injury (IRI) is a common complication in diverse clinical settings, including myocardial infarction, stroke, organ transplantation and major surgery. Its pathological core lies in the metabolic disruption caused by blood flow cessation, followed by oxidative stress, inflammatory cascades and cell death upon reperfusion. Aldehyde dehydrogenase 2 (ALDH2), a mitochondrial enzyme best known for its role in aldehyde detoxification, has emerged as an important endogenous protective factor in IRI. ALDH2 limits the accumulation of toxic lipid peroxidation products, preserves mitochondrial function and attenuates oxidative and inflammatory damage in multiple organs. In parallel, ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has been increasingly recognised as a key execution pathway in IRI. Increasing evidence suggests a close intersection between ALDH2 and ferroptosis. This review aims to systematically summarise the interplay between ALDH2 and ferroptosis in IRI, further explore their involvement in other forms of regulated cell death and highlight their points of convergence. Collectively, available data suggest that targeting ALDH2 may represent a promising strategy for limiting ferroptosis and reducing tissue damage in IRI.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512441","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

Regulation of Calcium Homeostasis by PIEZO1 Drives NETosis and Fibrosis in Bronchopulmonary Dysplasia 在支气管肺发育不良中，PIEZO1驱动NETosis和纤维化调控钙稳态。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-25 DOI: 10.1111/jcmm.71096

Lei Cao, Yan Mao, Chenxia Juan, Zhi Long, Qian Wang

{"title":"Regulation of Calcium Homeostasis by PIEZO1 Drives NETosis and Fibrosis in Bronchopulmonary Dysplasia","authors":"Lei Cao, Yan Mao, Chenxia Juan, Zhi Long, Qian Wang","doi":"10.1111/jcmm.71096","DOIUrl":"10.1111/jcmm.71096","url":null,"abstract":"Bronchopulmonary dysplasia (BPD) is a chronic lung disease primarily affecting preterm infants, characterised by impaired alveolar development and persistent inflammation, particularly associated with ventilator-induced lung injury due to mechanical ventilation. In this study, we performed an integrated bioinformatic analysis of multiple datasets (GSE108754 and GSE39840) and identified 203 differentially expressed genes (DEGs) between BPD and control samples. Functional enrichment analysis revealed significant involvement in cytokine-mediated signalling, response to lipopolysaccharide and regulation of interferon-beta production. Using machine learning algorithms (LASSO, SVM-RFE and Random Forest), we identified three hub genes (IL6, TFRC and PIEZO1) with high diagnostic accuracy for BPD. Immune infiltration analysis indicated altered immune cell proportions in BPD, with PIEZO1 expression positively correlated with neutrophil infiltration. Experimental validation confirmed elevated NETosis markers (PADI4, MPO, dsDNA) in BPD patients and further demonstrated that PIEZO1 overexpression promotes NET formation via calcium overload, which was inhibited by verapamil. Additionally, using a co-culture system, we showed that PIEZO1-induced NETosis exacerbates pulmonary fibrosis in lung epithelial cells. These findings highlight PIEZO1 as a key regulator of NETosis in BPD and a promising therapeutic target for mitigating lung injury and fibrosis.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512531","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 ‘Counteracting Skin Aging In Vitro by Phytochemicals’ 修正“植物化学物质在体外对抗皮肤老化”。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-25 DOI: 10.1111/jcmm.71114

引用次数: 0

Wogonin Mitigates Depression by Inhibiting TNF-α/TNFR1/CXCL1 Signalling-Mediated Astrocyte Activation Wogonin通过抑制TNF-α/TNFR1/CXCL1信号介导的星形细胞激活来缓解抑郁症。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-25 DOI: 10.1111/jcmm.71116

Huihui Chai, Kunying Zhao, Weiyan Hu, Bin Liu

{"title":"Wogonin Mitigates Depression by Inhibiting TNF-α/TNFR1/CXCL1 Signalling-Mediated Astrocyte Activation","authors":"Huihui Chai, Kunying Zhao, Weiyan Hu, Bin Liu","doi":"10.1111/jcmm.71116","DOIUrl":"10.1111/jcmm.71116","url":null,"abstract":"Wogonin exhibits notable anti-inflammatory and neuroprotective effects. Current study aimed to investigate the antidepressant potential of wogonin and its underlying mechanisms through in vitro and in vivo experiments. In vitro, wogonin attenuated lipopolysaccharide (LPS)-induced astrocyte activation. Furthermore, wogonin inhibited the TNF-α/TNFR1/CXCL1 signalling axis, as evidenced by decreased protein levels of TNF-α and CXCL1 and reduced interaction between TNF-α and its receptor TNFR1. The addition of recombinant TNF-α (r-TNF-α) blocked these inhibitory effects of wogonin. In vivo, in a chronic unpredictable mild stress (CUMS) mouse model, wogonin alleviated depression-like behaviours. Moreover, wogonin rescued CUMS-induced impairments in hippocampal synaptic plasticity, restoring post-tetanic potentiation (PTP), long-term potentiation (LTP) and mitigating neuronal damage in the CA1 region. Further analysis revealed that wogonin reduced levels of TNF-α and CXCL1 in both the hippocampal CA1 region and cerebrospinal fluid, and decreased the expression of astrocyte activation markers GFAP and C3. These effects of wogonin in vivo were reversed by co-administration of r-TNF-α and were replicated by treatment with the TNF-α inhibitor etanercept. These results demonstrate that wogonin may exert antidepressant effects by modulating the TNF-α/TNFR1/CXCL1 pathway, thereby improving neuroinflammation and astrocyte activation.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512498","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

Exploring Molecular Mechanism of Fluoxetine in Animal Models of Depression via Integrated Metabolomic and Proteomic Analysis 通过综合代谢组学和蛋白质组学分析探索氟西汀在抑郁症动物模型中的分子机制。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-25 DOI: 10.1111/jcmm.71112

Yin Chen, Wei Tang, Xiangkun Tao, Chi Liu, Hailin Wu, Ning Wang, Cenyu Liao, Nanxi He, Yiwen Chen, Yiyun Liu, Dongfang Wang, Siwen Gui, Xiaogang Zhong, Yuan Liu, Bin Hua, Lining Yang, Juncai Pu, Peng Xie

{"title":"Exploring Molecular Mechanism of Fluoxetine in Animal Models of Depression via Integrated Metabolomic and Proteomic Analysis","authors":"Yin Chen, Wei Tang, Xiangkun Tao, Chi Liu, Hailin Wu, Ning Wang, Cenyu Liao, Nanxi He, Yiwen Chen, Yiyun Liu, Dongfang Wang, Siwen Gui, Xiaogang Zhong, Yuan Liu, Bin Hua, Lining Yang, Juncai Pu, Peng Xie","doi":"10.1111/jcmm.71112","DOIUrl":"10.1111/jcmm.71112","url":null,"abstract":"Fluoxetine is a widely used antidepressant, yet integrated analyses of its molecular mechanism remain limited. This study systematically investigated potential molecular mechanisms underlying the antidepressant effects of fluoxetine by integrating these scattered data. Using the ProMENDA database, we identified metabolites and proteins altered by fluoxetine in the brain of animal models of depression. We curated 273 differentially expressed metabolite entries and 791 differentially expressed protein entries from fluoxetine treatment and performed vote-counting, pathway enrichment, pathway crosstalk and drug-associated metabolite set enrichment analyses. Vote-counting analysis showed altered neurotransmitter levels, including increased levels of monoamines and decreased levels of neurotoxic quinolinic acid and glutamate. The results of pathway analyses based on both altered metabolites and proteins showed 121 significantly enriched pathways. Pathway crosstalk analysis identified four pathway-based modules, which were mainly involved in amino acid metabolism, neurotransmitters and multiple biological processes. Drug-associated metabolite set enrichment analysis revealed 76 significantly enriched drug-related pathways, which were mainly involved in antidepressants. This study provides a comprehensive understanding of the antidepressant effects of fluoxetine, which may provide insights for the development of novel antidepressants.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512507","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

Old Blood, Young Bones: Identification of Middle-Aged Myeloid Cells That Limit Cortical Bone Loss 年老的血液，年轻的骨骼：限制皮质骨丢失的中年髓细胞的鉴定。

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-23 DOI: 10.1111/jcmm.71094

Jinsha Koroth, Ismael Y. Karkache, Elizabeth K. Vu, Joseph C. Manser, Mitchel J. Shimak, Kim C. Mansky, Elizabeth W. Bradley

{"title":"Old Blood, Young Bones: Identification of Middle-Aged Myeloid Cells That Limit Cortical Bone Loss","authors":"Jinsha Koroth, Ismael Y. Karkache, Elizabeth K. Vu, Joseph C. Manser, Mitchel J. Shimak, Kim C. Mansky, Elizabeth W. Bradley","doi":"10.1111/jcmm.71094","DOIUrl":"10.1111/jcmm.71094","url":null,"abstract":"Although studies support disrupted bone remodelling within geriatric populations, mid-life changes are understudied. To investigate this, we performed bone marrow transplantation assays using either 8- or 40-week-old mice. Micro-CT analyses of lethally irradiated 8-week-old mice transplanted with 40-week-old bone marrow exhibited increased mid-shaft femoral cortical bone mass and thickness. Intensive bone marrow regeneration mirrors hematopoietic development in that erythro-myeloid progenitors (EMPs) first expand to support blood production before definitive hematopoietic stem cell (HSC) production. We hypothesized that reduced HSC capacity of 40-week-old bone marrow and compensatory expansion of EMPs may facilitate gains in cortical bone. Flow cytometry analyses revealed greater EMP to HSC ratios when mice were reconstituted with increasing percentages of middle-aged bone marrow. To identify cell types mediating these effects, we performed comparative scRNA-Seq analyses and identified CD11B+CD36+ myeloid cells exhibiting enriched expression of bone anabolic cytokines. Elevated levels of Wnt ligands, especially Wnt6, characterized these cells. In lineage tracing assays, CD11B+CD36+ cells were donor-derived myeloid cells. In functional assays, we demonstrate that soluble factors produced by CD11B+CD36+ cells enhance osteogenesis. Moreover, CD11B/CD36/Wnt6 exquisitely mark anabolic macrophages within human bone marrow. These findings reveal a myeloid population present during midlife that enhances cortical bone.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504003","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

TSG101 Promotes SIAH1 Auto-Ubiquitination to Drive Migration and Invasion in Hepatocellular Carcinoma Cells TSG101促进SIAH1自身泛素化驱动肝癌细胞迁移和侵袭

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-23 DOI: 10.1111/jcmm.71109

Jie Qiu, Xixi Gu, Kai Wu, Jinzhao Wu, Chenrui Xu, Wengang Shan, Hengliang Shi

{"title":"TSG101 Promotes SIAH1 Auto-Ubiquitination to Drive Migration and Invasion in Hepatocellular Carcinoma Cells","authors":"Jie Qiu, Xixi Gu, Kai Wu, Jinzhao Wu, Chenrui Xu, Wengang Shan, Hengliang Shi","doi":"10.1111/jcmm.71109","DOIUrl":"10.1111/jcmm.71109","url":null,"abstract":"Our previous studies have demonstrated that seven in absentia homologue 1 (SIAH1), an E3 ubiquitin ligase, is downregulated in hepatocellular carcinoma (HCC) and regulates substrate ubiquitination. However, the molecular mechanisms governing reduced SIAH1 expression in HCC remain unclear. Here, a yeast two-hybrid experiment and co-immunoprecipitation assay identified tumour susceptibility gene 101 (TSG101) as a potential interacting protein of SIAH1. We found that TSG101 negatively regulated the expression of SIAH1. Besides, TSG101 is upregulated in HCC and associated with a poor prognosis. TSG101 promotes the migration and invasion of HCC cells by regulating SIAH1 expression. Molecularly, TSG101 promoted the auto-ubiquitination and degradation of SIAH1 via the proteasome pathway, thereby reducing its protein stability. Finally, the protein levels of SIAH1 were found to be inversely correlated with TSG101 in human HCC tissues. In summary, TSG101 is up-regulated in human HCC tissues and promotes the migration and invasion of HCC cells by inducing SIAH1 auto-ubiquitination and degradation.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503601","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

An Integrated Evaluation Framework for Adult Heart Regeneration 成人心脏再生的综合评价框架

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-23 DOI: 10.1111/jcmm.71099

Yixun Li, Xinchang Liu, Xianliang Zhou, Yu Nie, Jie Feng

{"title":"An Integrated Evaluation Framework for Adult Heart Regeneration","authors":"Yixun Li, Xinchang Liu, Xianliang Zhou, Yu Nie, Jie Feng","doi":"10.1111/jcmm.71099","DOIUrl":"10.1111/jcmm.71099","url":null,"abstract":"Myocardial infarction (MI) remains a primary global cause of mortality due to irreversible cardiomyocyte loss. While promoting endogenous regeneration offers a highly promising therapy, its validation is critically hindered by the lack of standardised, comprehensive methodologies for quantitative assessment. To address this, we developed an integrated, systematically validated experimental framework for the precise evaluation of heart regeneration after ischemic injury in adult mice. This framework standardises four key assessment dimensions: (1) serial echocardiography mapping for precise serial evaluation of left ventricular function and structural changes; (2) standardised Masson's trichrome staining with systematic transverse sampling across five sections for reproducible quantification of post-ischemic scar burden; (3) stringent multi-marker strategy (EdU, pH 3 and Aurora B) for the accurate quantification of cardiomyocyte cell-cycle reactivation; (4) total cardiomyocyte enumeration achieved by employing enzymatic digestion to derive definitive quantitative metrics, confirming successful cell replenishment. This integrated framework establishes detailed and reproducible methodological standards to significantly enhance the accuracy and reliability of heart regeneration research. It thereby provides a robust reference for the standardised assessment of heart regeneration in adult mice.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498521","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

Association Between Lactate and ICU-Acquired Infection in Critically Ill Patients With Sepsis: A Retrospective Study Using the MIMIC-IV Database 危重症脓毒症患者乳酸与icu获得性感染的关系：使用MIMIC-IV数据库的回顾性研究

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-03-23 DOI: 10.1111/jcmm.71090

Yue Zhao, Lu Yao, Jiaji Fu, Mei He, Peichi Shi, Jiqian Xu, You Shang

{"title":"Association Between Lactate and ICU-Acquired Infection in Critically Ill Patients With Sepsis: A Retrospective Study Using the MIMIC-IV Database","authors":"Yue Zhao, Lu Yao, Jiaji Fu, Mei He, Peichi Shi, Jiqian Xu, You Shang","doi":"10.1111/jcmm.71090","DOIUrl":"10.1111/jcmm.71090","url":null,"abstract":"Sepsis is a leading cause of Intensive Care Unit (ICU) mortality, often complicated by secondary infections due to sepsis-induced immunosuppression. The ICU-acquired infection (IAI) is of particular concern in severe cases, as it heightens the risk of progression to chronic critical illness (CCI). Given the scarcity of established biomarkers for IAI, this study aimed to evaluate the potential association of early blood lactate levels, a recognised prognostic marker in sepsis, with the occurrence of this complication. We conducted a retrospective analysis of data from the Medical Information Mart for Intensive Care (MIMIC)-IV database (v3.0), enrolling 17,209 patients. The cohort had a median age of 67 years (IQR, 56–77) and a median admission lactate level of 2.6 mmol/L (IQR, 1.6–4.8). Our analysis revealed a linear dose–response relationship between admission lactate levels and IAI risk. After multivariable adjustment, hyperlactatemia (> 6 mmol/L, i.e., the group with the highest lactate levels, Q5) remained independently associated with increased odds of IAI (OR = 1.36; 95% CI, 1.08–1.70). Notably, while elevated lactate predicted higher 28-day ICU mortality in patients without IAI, this relationship was not maintained in the IAI cohort following multivariable adjustment.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71090","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503968","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