Life sciences最新文献

{"title":"Extracellular vesicles from mesenchymal stem cells improve liver injury in rats with mild liver damage. Underlying mechanisms and role of TGFβ","authors":"Gergana Mincheva ,&nbsp;Victoria Moreno-Manzano ,&nbsp;Vicente Felipo ,&nbsp;Marta Llansola","doi":"10.1016/j.lfs.2025.123429","DOIUrl":"10.1016/j.lfs.2025.123429","url":null,"abstract":"<div><div>Preventing the progression of liver damage to fibrosis would be beneficial for patients with steatotic liver disease (SLD). Mesenchymal stem cells (MSC) are a promising therapy for SLD and derived extracellular vesicles (EVs) could even improve the treatment's efficacy and safety. However, the mechanisms of MSC-EVs beneficial effects are not well known. It has been suggested that modifying the EVs cargo could improve their beneficial effects. The aims of this study were to assess if MSC-EVs reduce liver damage in a rat model of mild liver damage; to analyze the underlying mechanisms and to assess if silencing TGFβ enhances the beneficial effects of MSC-EVs. CCl₄ was injected three times per week during four weeks to induce mild liver damage. EVs from human adipocyte MSC and from TGFβ-depleted MSC (siTGFβ-MSC-EVs) were injected in the tail vein. Steatosis, fibrosis, liver inflammation, macrophage infiltration and liver content of fibrotic markers, DAMPs, cytokines and bile acids were analyzed. Normal MSC-EVs reduce the CCL2 increase in liver, macrophage infiltration and the increases in the fibrosis markers collagen I and α-SMA. Treatment with siTGFβ-MSC-EVs, in addition, reduces liver steatosis, the increase of bile acids (mainly TCA), and DAMP HMGB1 levels, inducing a larger reduction of collagen I in liver of CCl₄ rats.</div><div>Treatment with MSCs-EVs effectively reduces early liver damage. Silencing of TGFβ in MSCs enhances the beneficial effects by additional mechanisms. Early treatment with MSC-EVs, especially after silencing TGFβ, could improve liver damage in SLD patients.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123429"},"PeriodicalIF":5.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of megakaryocytic leukemia 1 in endothelial cells contributes to diabetic retinopathy in mice","authors":"Yuwen Zhu ,&nbsp;Xiaofen Feng ,&nbsp;Fei Wang ,&nbsp;Yuhua Ding","doi":"10.1016/j.lfs.2025.123425","DOIUrl":"10.1016/j.lfs.2025.123425","url":null,"abstract":"<div><h3>Aims</h3><div>Diabetic retinopathy (DR) represents one of the most devastating sequences in patients with diabetes. Endothelial dysfunction is a key pathological feature of and contributing factor to DR. In the present study we investigated the role of megakaryocytic leukemia 1 (MKL1) in DR pathogenesis.</div></div><div><h3>Methods and materials</h3><div>DR was induced in mice by feeding with a high-fat diet (HFD). The <em>Mkl1</em>-Rosa26-KI mice were crossed to the <em>Cdh5</em>-Cre^ERT2 mice to generate endothelial-specific MKL1 knock-in mice (MKL1^EC-KI).</div></div><div><h3>Key findings</h3><div>In cultured human primary retinal endothelial cells exposure to high glucose promoted nuclear translocation of MKL1 without altering its mRNA or protein expression. MKL1 knockdown ameliorated whereas MKL1 over-expression exacerbated high glucose induced impairment of endothelial barrier function. Compared to wild type littermates, MKL1^EC-KI mice fed on HFD displayed worsened insulin resistance and accelerated DR pathogenesis. Consistently, administration of an MKL1 inhibitor CCG-1423 protected the mice from HFD feeding induced metabolic disorders and DR pathogenesis.</div></div><div><h3>Significance</h3><div>Our data demonstrate that MKL1 may contribute to diabetic retinopathy by regulating endothelial behavior. Targeting MKL1 with small-molecule inhibitors can be considered as a therapeutic solution for the treatment of diabetic retinopathy.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123425"},"PeriodicalIF":5.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cold and longevity: Can cold exposure counteract aging?","authors":"Ayoub Boulares,&nbsp;Hela Jdidi,&nbsp;Wafa Douzi","doi":"10.1016/j.lfs.2025.123431","DOIUrl":"10.1016/j.lfs.2025.123431","url":null,"abstract":"<div><div>Aging is a multifaceted biological process characterized by a progressive decline in physiological functions and heightened vulnerability to diseases, shaped by genetic, environmental, and lifestyle factors. Among these, cold exposure has garnered interest for its potential anti-aging benefits. This review examines the impact of cold exposure on aging, focusing on key physiological processes such as inflammation, oxidative stress, metabolic regulation, and cardiovascular health. Cold exposure has been shown to reduce chronic inflammation, enhance antioxidant defenses, and improve metabolic health by activating brown adipose tissue. Furthermore, findings from hibernating mammals and model organisms suggest a connection between lower environmental temperatures and increased longevity. However, the potential long-term health risks of extended cold exposure, particularly in older adults, remain a significant concern. Epidemiological studies reveal increased rates of mortality and morbidity in populations living in cold climates, emphasizing the complexity of the relationship between cold exposure and aging. This review underscores the need for further research to elucidate the long-term effects of cold exposure on aging and to establish guidelines for leveraging its benefits while mitigating cold-induced risks.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123431"},"PeriodicalIF":5.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiation exposure in neurosurgical intensive care unit patients: Balancing diagnostic benefits and long-term risks","authors":"A. Grote ,&nbsp;M. Bopp ,&nbsp;F. Stelten ,&nbsp;A. Kemmling ,&nbsp;B. Carl ,&nbsp;Ch. Nimsky","doi":"10.1016/j.lfs.2025.123426","DOIUrl":"10.1016/j.lfs.2025.123426","url":null,"abstract":"<div><h3>Background</h3><div>X-ray, computed tomography (CT), and digital subtraction angiography (DSA) techniques are indispensable in managing critically ill neurosurgical patients. However, repeated diagnostic imaging leads to cumulative radiation exposure, raising concerns about long-term risks such as malignancies. This study evaluates the frequency, dosage, and implications of radiation exposure in a neurosurgical intensive care unit (NICU) patient cohort.</div></div><div><h3>Methods</h3><div>A retrospective analysis was conducted on 589 patients admitted to the NICU between 2013 and 2018 with the diagnosis of traumatic brain injury (TBI), intracerebral hemorrhage (ICH), subarachnoidal hemorrhage (SAH), and stroke with &gt;24 h of mechanical ventilation time. The cumulative radiation dose per patient from X-ray, CT, and DSA imaging was calculated and stratified by diagnostic indication, patient condition, and clinical course. To contextualize the findings, international benchmarks were compared.</div></div><div><h3>Results</h3><div>The cohort's median cumulative effective dose (ED) was 17.8 mSv (range: 1.7–194.3 mSv). CT scans accounted for 81.95 % of the total radiation exposure, with head and thorax imaging being the most frequently performed studies. Younger age and a shorter ventilation time revealed a significant increase in the calculated lifetime attributable risk (LAR) of radiation-induced cancer in multivariate testing. Comparisons with international data revealed a comparable level of radiation exposure in this cohort. Despite the high radiation burden, imaging was deemed clinically essential, with direct implications for patient outcomes.</div></div><div><h3>Conclusion</h3><div>While radiation exposure in NICU patients is substantial, the benefits of timely and accurate diagnostic information outweigh the potential long-term risks. In critical care settings, where patients face life-threatening conditions, the judicious use of diagnostic imaging is essential. Future efforts should focus on optimizing imaging protocols to minimize radiation exposure without compromising diagnostic quality.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123426"},"PeriodicalIF":5.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a novel fibroblast growth factor receptor-agonistic peptide and its effect on diabetic wound healing","authors":"Mariya Farooq ,&nbsp;Moonjung Hwang ,&nbsp;Abdul Waheed Khan ,&nbsp;Maria Batool ,&nbsp;Bilal Ahmad ,&nbsp;Wook Kim ,&nbsp;Moon Suk Kim ,&nbsp;Sangdun Choi","doi":"10.1016/j.lfs.2025.123432","DOIUrl":"10.1016/j.lfs.2025.123432","url":null,"abstract":"<div><h3>Aims</h3><div>Fibroblast growth factor (FGF) is a broad class of secretory chemicals that act <em>via</em> FGF receptors (FGFR). The study aims to explore the role of a novel peptide, FAP1 (FGFR-agonistic peptide 1), in tissue regeneration and repair. It investigates whether FAP1 mimics basic fibroblast growth factor (bFGF) and accelerates wound healing both <em>in vitro</em> and <em>in vivo</em>.</div></div><div><h3>Main methods</h3><div>In this study, a novel peptide was designed and its ability to mimic bFGF was assessed through different <em>in vitro</em> experiments including its effect on cell proliferation, wound healing, cell signaling including FGFR1 phosphorylation and activation of mitogen-activated protein kinases (MAPKs). Specificity was confirmed through surface plasmon resonance (SPR) analysis and co-treatment with FGFR inhibitor, erdafitinib. <em>In vivo</em>, the effect of FAP1 on diabetic wound healing was tested in a mouse model, examining collagen production and the migration and proliferation of keratinocytes and fibroblasts.</div></div><div><h3>Key findings</h3><div>FAP1 specifically phosphorylated FGFR and activated MAPKs similar to bFGF. <em>In vitro</em>, it induced cell proliferation and accelerated wound healing. <em>In vivo</em>, FAP1 improved diabetic wound healing by increasing collagen production and promoting keratinocyte and fibroblast migration and proliferation. The specificity of FAP1 was confirmed through SPR.</div></div><div><h3>Significance</h3><div>FAP1 shows potential as a novel pharmacological alternative to natural bFGF for skin tissue regeneration and repair. Its ability to accelerate wound healing and its specificity for FGFR suggest that FAP1 could serve as a cost-effective substitute for bFGF protein in therapeutic applications.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123432"},"PeriodicalIF":5.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperoside mitigates PCOS-associated adipogenesis and insulin resistance by regulating NCOA2-mediated PPAR-γ ubiquitination and degradation","authors":"Qi Zhou ,&nbsp;Hong Tang ,&nbsp;Yongfeng Wang ,&nbsp;Yu Hua ,&nbsp;Xiaoling Ouyang ,&nbsp;Linxia Li","doi":"10.1016/j.lfs.2025.123417","DOIUrl":"10.1016/j.lfs.2025.123417","url":null,"abstract":"<div><h3>Aims</h3><div>Polycystic ovary syndrome (PCOS) is closely associated with metabolic disorders such as insulin resistance and obesity, but the role of adipogenesis in its pathophysiology remains unclear. This study investigates the role of adipogenesis in PCOS development and evaluates whether hyperoside (HPS), an anti-adipogenic herbal compound, can improve PCOS by inhibiting adipogenesis.</div></div><div><h3>Main methods</h3><div>A combination of in vivo and in vitro models was used to assess the impact of HPS on ovarian function, insulin resistance, and adipogenesis. PCOS mice were treated with HPS, and their ovarian function and insulin resistance were evaluated. In vitro adipocyte differentiation assays were conducted to examine the effects of HPS on adipogenesis. The target of HPS was analyzed by Surface plasmon resonance. The expression levels of NCOA2 and PPAR-γ ubiquitination and degradation were analyzed using quantitative real-time PCR and Western blotting. Additionally, NCOA2 knockdown experiments were performed to investigate its role in ovarian function, insulin resistance, and adipogenesis in PCOS mice.</div></div><div><h3>Key findings</h3><div>HPS treatment significantly improved ovarian function, reduced insulin resistance, and suppressed adipogenesis in PCOS mice. Mechanistically, HPS inhibited adipogenesis by reducing NCOA2 expression, thereby preventing PPAR-γ ubiquitination and degradation. Knockdown of NCOA2 further validated its role by improving ovarian function, insulin resistance, and adipogenesis in PCOS models.</div></div><div><h3>Significance</h3><div>These findings demonstrate that HPS alleviates PCOS by regulating NCOA2-mediated PPAR-γ ubiquitination and degradation, offering new insights into the role of adipogenesis in PCOS pathophysiology.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"364 ","pages":"Article 123417"},"PeriodicalIF":5.2,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and regulation of a novel leptin receptor-linked enhancer during zebrafish ventricle regeneration","authors":"Qi Li ,&nbsp;Yan Zhao ,&nbsp;Fang Geng ,&nbsp;Xiamisiya Tuniyazi ,&nbsp;Chunxiao Yu ,&nbsp;Hongbo Lv ,&nbsp;Hongbo Yang ,&nbsp;Ruilin Zhang","doi":"10.1016/j.lfs.2025.123415","DOIUrl":"10.1016/j.lfs.2025.123415","url":null,"abstract":"<div><h3>Aims</h3><div>Vertebrates vary greatly in their abilities to regenerate injured hearts. Zebrafish possess a remarkable capacity for cardiac regeneration, making them an excellent model for regeneration research. Recent studies have reported the activation and underlying regulatory mechanisms of <em>leptin b</em> (<em>lepb</em>) and the <em>leptin b</em>-linked enhancer (<em>LEN</em>) in injured hearts. However, the regenerative response activity of the <em>leptin receptor</em> (<em>lepr</em>) and its regulatory mechanisms still warrant further exploration.</div></div><div><h3>Materials and methods</h3><div>We identified a novel <em>lepr</em>-linked enhancer (<em>leprEnh</em>) and generated a stable transgenic zebrafish line for validation. We also employed a genetic ventricle ablation system to elucidate the mechanisms governing its activation. Immunofluorescence, <em>in situ</em> hybridization and confocal imaging of larvae treated with various inhibitors during ventricle regeneration were performed.</div></div><div><h3>Key findings</h3><div>Our results revealed that both <em>lepr</em> expression and <em>leprEnh</em>-directed EGFP fluorescence were weakly expressed in the ventricle during early heart development but displayed a sharp increase after ventricle ablation. Strong injury response activity was also observed in the atrium. Furthermore, the regeneration-responsive activity was attenuated by hemodynamic force alteration and was modulated by Notch, ErbB2 and BMP signaling pathways.</div></div><div><h3>Significance</h3><div>Our study sheds light on the regulation of <em>lepr</em> and <em>leprEnh</em> during heart regeneration and provide a basis for screening for novel therapeutic targets for myocardial infarction.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"363 ","pages":"Article 123415"},"PeriodicalIF":5.2,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reproductive outcomes in female mice offspring due to maternal metformin treatment","authors":"Candela Velazquez ,&nbsp;Yamila Herrero ,&nbsp;Katherine Prost ,&nbsp;Mayra Bordaquievich ,&nbsp;Melanie Neira ,&nbsp;Fernanda Parborell ,&nbsp;Dalhia Abramovich","doi":"10.1016/j.lfs.2025.123416","DOIUrl":"10.1016/j.lfs.2025.123416","url":null,"abstract":"<div><h3>Aims</h3><div>Metformin has shown beneficial effects on reproduction in women. However, its use during pregnancy remains controversial, as metformin can cross the placenta. Most studies have focused on the metabolic impact on the offspring of treated mothers, with limited information regarding its reproductive effects. The aim of this study was to evaluate potential alterations in ovarian function and fertility in female offspring of mothers treated with metformin during pregnancy and lactation.</div></div><div><h3>Materials and methods</h3><div>C57BL/6 female mice were treated with metformin four weeks before mating, and the treatment was maintained during gestation and lactation. Seven weeks after weaning, metabolic parameters as well as ovarian and reproductive function of the offspring were analyzed.</div></div><div><h3>Key findings</h3><div>The offspring of treated mothers were lighter at birth and, in adulthood, they had more gonadal adipose tissue with no alterations in body weight. No changes in glucose metabolism were observed. Their follicular development was modified, with more early antral and atretic follicles and less primary and late antral follicles. Anti-Müllerian hormone expression and ovarian angiogenesis were increased. The estrous cycle, hormonal production and fertility were not affected by metformin exposure, however, the F2 generation showed higher body weight at birth.</div></div><div><h3>Significance</h3><div>Metformin can induce fetal programming in animals exposed to it during development, impacting metabolism and ovarian functionality in adulthood. Under physiological conditions, these alterations do not result in reduced fertility or endocrine disruptions. Our data warrant studies in women to make informed decisions regarding metformin administration during critical developmental periods in clinical settings.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"363 ","pages":"Article 123416"},"PeriodicalIF":5.2,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell–cell communications in the brain of hepatic encephalopathy: The neurovascular unit","authors":"Kyuwan Choi ,&nbsp;Yena Cho ,&nbsp;Yerin Chae ,&nbsp;So Yeong Cheon","doi":"10.1016/j.lfs.2025.123413","DOIUrl":"10.1016/j.lfs.2025.123413","url":null,"abstract":"<div><div>Many patients with liver diseases are exposed to the risk of hepatic encephalopathy (HE). The incidence of HE in liver patients is high, showing various symptoms ranging from mild symptoms to coma. Liver transplantation is one of the ways to overcome HE. However, not all patients can receive liver transplantation. Moreover, patients who have received liver transplantation have limitations in that they are vulnerable to hepatocellular carcinoma, allograft rejection, and infection. To find other therapeutic strategies, it is important to understand pathological factors and mechanisms that lead to HE after liver disease. Oxidative stress, inflammatory response, hyperammonaemia and metabolic disorders seen after liver diseases have been reported as risk factors of HE. These are known to affect the brain and cause HE. These peripheral pathological factors can impair the blood-brain barrier, cause it to collapse and damage the neurovascular unit component of multiple cells, including vascular endothelial cells, astrocytes, microglia, and neurons, leading to HE. Many previous studies on HE have suggested the impairment of neurovascular unit and cell–cell communication in the pathogenesis of HE. This review focuses on pathological factors that appear in HE, cell type-specific pathological mechanisms, miscommunication/incorrect relationships, and therapeutic candidates between brain cells in HE. This review suggests that regulating communications and interactions between cells may be important in overcoming HE.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"363 ","pages":"Article 123413"},"PeriodicalIF":5.2,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the physiological mechanisms and therapeutic targets of diseases: Lipidomics strategies","authors":"Qiang Yang ,&nbsp;Ying Cai ,&nbsp;Zhibo Wang ,&nbsp;Sifan Guo ,&nbsp;Shi Qiu ,&nbsp;Aihua Zhang","doi":"10.1016/j.lfs.2025.123411","DOIUrl":"10.1016/j.lfs.2025.123411","url":null,"abstract":"<div><div>As a pivotal branch of metabolomics, lipidomics studies global changes in lipid metabolism under different physiological and pathological conditions or drug interventions, discovers key lipid markers, and elaborates the associated lipid metabolism network. There are a considerable number of lipids in the host, which act on various functional networks such as metabolism and immune regulation. As an indispensable research method, lipidomics plays a key character in the analysis of lipid composition in organisms, the elaboration of the physiological mechanism of lipids, and the decoding of their character in the occurrence and development of diseases by exploring the character of lipids in the host environmental network. As an essential means of driving lipidomics research, High-throughput and High-resolution mass spectrometry is helpful in exploring disease phenotypic characteristics, diagnosing disease biomarkers, regulating related metabolic pathways, and discovering related active components. In this paper, we discuss the specific role of lipidomics in the analysis of disease diagnosis, prognosis and treatment, which is conducive to the realization of accurate and personalized medicine.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"363 ","pages":"Article 123411"},"PeriodicalIF":5.2,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}