Cell Biochemistry and Function最新文献

{"title":"Subacute Exposure to Aldrin, Endosulfan and Lindane Differentially Alters Metabolic and Inflammatory Gene Expression in White and Brown Adipose Tissue of Male Rats","authors":"Nada Abdelhamid Mohamed Boujanah,&nbsp;Cihan Suleyman Erdogan,&nbsp;Engin Sumer,&nbsp;Cansu Yakin,&nbsp;Bayram Yilmaz","doi":"10.1002/cbf.70262","DOIUrl":"https://doi.org/10.1002/cbf.70262","url":null,"abstract":"<p>Persistent organic pollutants such as organochlorine pesticides (OCPs) have been implicated in obesity and metabolic dysfunction. As they bioaccumulate in adipose tissue, OCPs may act as obesogens, but in vivo evidence for aldrin, endosulfan and lindane is limited. This study investigated whether subacute exposure to aldrin, endosulfan and lindane elicits obesogenic effects in male rats by examining weight gain, serum biochemistry and metabolic and inflammatory gene expression in white adipose tissue (WAT) and brown adipose tissue (BAT). Thirty-two adult male Sprague-Dawley rats were randomly assigned to receive corn oil (control) or oral aldrin, endosulfan or lindane (1 mg/kg every other day for 28 days). Body weight was recorded weekly. Serum liver enzymes and lipid profile were determined. In WAT and BAT, we quantified mRNA expression of thermogenic and adipogenic markers (<i>Pparg</i>, <i>Ucp1</i>, <i>Ucp3</i>, <i>Fndc5</i>), and the pro- and anti-inflammatory cytokines (<i>Il-1b</i>, <i>Tnf-α</i>, <i>Il-10</i>, <i>Il-4</i>). Lindane caused significant weight gain from the first week (<i>p</i> &lt; 0.0001), whereas aldrin and endosulfan increased body weight only at week four (<i>p</i> &lt; 0.05). Endosulfan-treated rats had reduced total and high-density lipoprotein cholesterol (<i>p</i> &lt; 0.05) without changes in low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, or triglycerides. In WAT, <i>Pparg</i>, <i>Ucp1</i>, and <i>Fndc5</i> transcripts were unchanged, while <i>Ucp3</i> tended to decrease in the endosulfan group (<i>p</i> = 0.056). In BAT, endosulfan increased <i>Ucp1</i> and decreased <i>Fndc5</i> levels (<i>p</i> &lt; 0.05), with no changes in <i>Pparg</i> or <i>Ucp3</i>. Endosulfan suppressed <i>Il-1b</i>, <i>Tnf-α</i>, and <i>Il-10</i> (<i>p</i> &lt; 0.05) transcripts in both WAT and BAT, and all pesticides reduced <i>Il-4</i> expression in BAT (<i>p</i> &lt; 0.05). Overall, short-term exposure to aldrin, endosulfan or lindane interfered with metabolic and inflammatory pathways in a compound-specific manner, with lindane causing early weight gain and endosulfan eliciting complex effects on lipid metabolism and adipose gene expression. We suggest that even short-term exposure to OCPs may affect metabolic regulation in male rats, with each chemical exerting distinct effects.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epithelial–Mesenchymal Plasticity in Cancer: Transcriptional Regulation, Biomarker Challenges, and Emerging Therapeutic Opportunities","authors":"Dhrruv Shah,&nbsp;Rajasekhar Reddy Alavala","doi":"10.1002/cbf.70271","DOIUrl":"https://doi.org/10.1002/cbf.70271","url":null,"abstract":"<div>\u0000 \u0000 <p>Epithelial–mesenchymal transition (EMT) is increasingly recognized as a dynamic process of epithelial–mesenchymal plasticity (EMP) rather than a binary switch between epithelial and mesenchymal phenotypes. This plasticity enables tumor cells to acquire invasive, metastatic, stem-like, and therapy-resistant characteristics that contribute to cancer progression and poor clinical outcomes. Despite extensive investigation, significant challenges remain in understanding the functional significance of partial EMT states, identifying robust biomarkers that capture EMT heterogeneity, and translating EMT-targeted interventions into clinical practice. This review critically examines the molecular mechanisms governing EMT, including transcriptional regulators, signaling pathways, epigenetic modifications, and tumor microenvironmental influences. Particular emphasis is placed on hybrid epithelial/mesenchymal states, which have emerged as key drivers of metastatic fitness and therapeutic resistance. We further evaluate established and emerging EMT biomarkers, including E-cadherin, N-cadherin, vimentin, circulating tumor cells, and exosome-derived signatures, highlighting their opportunities and limitations in clinical applications. Finally, we discuss current therapeutic strategies targeting EMT-associated pathways and explain why many promising preclinical approaches have faced translational barriers. By integrating mechanistic, biomarker, and therapeutic perspectives, this review proposes that understanding and targeting epithelial–mesenchymal plasticity, rather than EMT alone, may provide a more effective framework for precision oncology and metastasis prevention.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thermodynamic Frontiers in Hemoglobin-Inspired Polymer Science for Diagnosis and Modulation of Neurodegenerative Diseases","authors":"Mohammad Edrisi,&nbsp;Navid Rabiee","doi":"10.1002/cbf.70261","DOIUrl":"10.1002/cbf.70261","url":null,"abstract":"<div>\u0000 \u0000 <p>The thermodynamic logic underlying hemoglobin's cooperative binding and reversible conformational transitions offers a powerful conceptual model for reimagining polymer design in neurodegenerative medicine. In this review perspective, we outline a unified thermodynamic framework that connects molecular energetics, polymer science, and pathological protein aggregation. We discuss how hemoglobin's allosteric adaptability, enthalpy–entropy compensation, and redox responsiveness can inspire polymers capable of sensing and reshaping the free-energy landscapes that govern amyloid formation. Drawing on evidence from protein thermodynamics, polymer chemistry, and neurobiological systems, we propose design principles for adaptive, hemoglobin-inspired polymers that act as artificial chaperones, materials capable of modulating aggregation equilibria, restoring proteostatic balance, and integrating diagnostic and therapeutic functions. This article defines an emerging field at the intersection of thermodynamic polymer science and neurodegeneration, where materials are not passive carriers but active regulators of molecular energy landscapes.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Fatty Acid Oxidation in Crohn's Disease and Ulcerative Colitis: Metabolomics Analysis and Experimental Evidence","authors":"Fang Yan,&nbsp;Shimin Wu,&nbsp;Wenqiang Yuan,&nbsp;Qian Yang,&nbsp;Jie Yang,&nbsp;Dejun Cui","doi":"10.1002/cbf.70246","DOIUrl":"https://doi.org/10.1002/cbf.70246","url":null,"abstract":"<div>\u0000 \u0000 <p>The metabolic determinants that distinguish Crohn's disease (CD) from ulcerative colitis (UC) and their roles in driving immune dysregulation remain elusive. We aimed to identify systemic metabolic signatures of inflammatory bowel disease (IBD) and elucidate the mechanistic link between metabolite availability and regulatory T cell (Treg) homeostasis. We performed untargeted LC-MS-based metabolomics on plasma from patients with <i>CD</i> (<i>n</i> = 17), <i>UC</i> (<i>n </i>= 13), and healthy controls (<i>n</i> = 15). Pathway enrichment and topology analysis were used to identify perturbed biological processes. The functional role of identified metabolites was validated using primary murine naive CD4⁺ <i>T cell</i> differentiation assays, Seahorse XF metabolic flux analysis, and siRNA-mediated knockdown. The therapeutic relevance was assessed in a DSS-induced murine model of colitis. Metabolomic profiling identified 175 significant differential metabolites, revealing a profound systemic depletion of fatty acids and a specific deficit in the fatty acid oxidation (FAO) pathway in <i>CD</i> patients. Palmitic acid and butyrate emerged as robust diagnostic biomarkers (AUC = 0.877–0.975). In vitro, butyrate dose-dependently promoted iTreg differentiation by increasing the oxygen consumption rate and maximal respiratory capacity. This effect was dependent on carnitine palmitoyltransferase 1A (CPT1A), as pharmacological or genetic inhibition of <i>CPT1A</i>-mediated <i>FAO</i> abolished butyrate's pro-differentiation capacity. In vivo, the ability of butyrate to attenuate colitis and promote colonic iTreg accumulation was significantly reversed by the <i>CPT1</i> inhibitor etomoxir. <i>CPT1A</i>-mediated fatty acid oxidation is a critical metabolic pivot through which butyrate signals to maintain immune tolerance. The systemic loss of <i>FAO</i> intermediates in <i>CD</i> patients directly contributes to impaired iTreg development, identifying the butyrate–<i>CPT1</i>A axis as a potential target for precision metabolic intervention.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phytohemagglutinin: A Tool for Inducing Neuroinflammation Mediated In Vitro and In Vivo Modeling of Alzheimer's Disease Pathology","authors":"Sarosh Farooq Khan,&nbsp;Maha Shahid,&nbsp;Shabana Usman Simjee","doi":"10.1002/cbf.70269","DOIUrl":"https://doi.org/10.1002/cbf.70269","url":null,"abstract":"<div>\u0000 \u0000 <p>Alzheimer's disease (AD) is an irreversible neurodegenerative disorder and the major cause of dementia globally. One of the major barriers to curing AD is the lack of experimental models that fully recapitulate the complexity of human AD pathology. Evidence supports the notion that neuroinflammation is a key pathological contributing factor of AD. Therefore, various external stimuli are used to recapitulate the AD-like pathology, i.e., LPS, scopolamine, and aluminum chloride. Although PHA is reported for its pro-inflammatory activity, using PHA to recapitulate the AD-like pathology is relatively new. The current study was designed to evaluate the PHA potential to recapitulate the AD-like pathology in primary neuronal culture as well as in vivo AD modeling. Since LPS is widely used, in the current study, it was used to compare it with the experimental findings using PHA. Confirmation of AD-like pathology was carried out through gene and protein expression in the in vitro study, while in vivo results were verified through behavioral and histopathological assays. It was observed that PHA mimics the AD-like pathology at the cellular level by aggregating, shrinking, and disrupting synaptic plasticity of primary neuronal cells. An elevated level of <i>BACE1</i> and amyloid-β and hyperphosphorylated tau protein expression, along with reduced levels of the ADAM10 gene, evidently proves that PHA induces the AD-like pathology. Disrupted cognitive and memory patterns confirm the initiation of AD pathogenesis in the in vivo study, which is further confirmed by observing the amyloid plaques stained by Congo red (CR) dye. Based on these findings, it is concluded that PHA is a potent inducer to recapitulate neuroinflammatory-mediated AD-like pathology both in vitro and in vivo.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ADAM20 Participates Modestly to Fertilization as Its Absence Leads to In Vitro Hypofertility in Mouse","authors":"Marie-Sophie Girault,&nbsp;Sophie Dupuis,&nbsp;Rémi Pierre,&nbsp;Christine Gourier,&nbsp;Jeffrey E. Lee,&nbsp;Sandrine Barbaux,&nbsp;Ahmed Ziyyat","doi":"10.1002/cbf.70265","DOIUrl":"10.1002/cbf.70265","url":null,"abstract":"<div>\u0000 \u0000 <p>A mutation of the <i>ADAM20</i> gene was described in an infertile patient whose spermatozoa were observed accumulating in the perivitelline space of oocytes. To decipher its role in the fertilization process, we produced a mouse model knock-out (KO) for the <i>Adam20</i> gene. Surprisingly, <i>Adam20</i>-KO males showed an in vivo fertility similar to their wild-type littermates and had normal sperm counts and morphology. However, they presented a reduced fertility in in vitro fertilization assays. To explore the hypothesis that the two flanking genes <i>Adam25</i> and <i>Adam39</i> could compensate the lack of <i>Adam20</i> given their very high homology, we produced a triple KO deleting these three neighbor genes simultaneously. The phenotype was strictly identical to that of the single gene deletion. Therefore, ADAM20, ADAM25, and ADAM39 are not essential proteins for fertilization in mice but they seem to participate modestly to the process. <i>Adam20</i>-KO males are fertile in vivo but have a reduced fertility in vitro. Males deleted for three neighbor and very homologous genes (<i>Adam20</i>, <i>Adam25</i>, and <i>Adam39</i>) have the same phenotype as the simple <i>Adam20</i>-KO. These genes are dispensable for normal fertility but contribute modestly to fertilization.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two-Way Communication Between Skeletal Muscle and Myokines","authors":"Tengteng Huang,&nbsp;Shihao Zhou,&nbsp;Xiaoling Chen,&nbsp;Daiwen Chen,&nbsp;Bing Yu,&nbsp;Zhiqing Huang","doi":"10.1002/cbf.70267","DOIUrl":"10.1002/cbf.70267","url":null,"abstract":"<div>\u0000 \u0000 <p>Myokines are defined as a class of bioactive molecules—including metabolites, peptides, and proteins—released from skeletal muscle cells and promoted by exercise. Recently, myokine-mediated muscle-organ crosstalk has sparked increased interest. Skeletal muscle secretes hundreds of myokines in an autocrine, paracrine, or endocrine manner, mediating the crosstalk between skeletal muscle and skeletal muscle itself, bone, fat, liver, and so on to regulate the physiological state of multiple organs, exerting a wide range of benefits of exercise. The relationship between muscle and myokines may be better understood as an exercise-responsive regulatory framework involving skeletal muscle and myokines, although direct evidence for an integrated bidirectional feedback network remains incomplete. In the network, myokines regulate skeletal muscle metabolism and remodeling through autocrine/paracrine actions, while exercise-induced muscle-derived signals may also contribute to long-lasting systemic adaptations involving immune mobilization, redox homeostasis, gut microbiota-related metabolic remodeling, and gut-muscle-bone crosstalk. Therefore, the distinct feature of skeletal muscle is not the mere presence of bidirectional signaling but its large mass, fiber-type metabolic heterogeneity, and direct responsiveness to repeated mechanical stimuli during exercise. On the one hand, as a source of myokines, the stimulation of skeletal muscle affects the production of myokines through various signaling pathways. On the other hand, myokines affect skeletal muscle function, such as glucose absorption, fatty acid oxidation, skeletal muscle mass, and muscle fiber type transformation. What's more, some myokines are muscle fiber type-specific, meaning that the expression of myokines may be influenced by muscle fiber type. Based on these, this review aims to summarize current evidence for exercise-responsive interactions between skeletal muscle and myokines and to identify where feedback regulation remains hypothetical.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research Progress on the ARHGEF Family in Cardiovascular Diseases","authors":"Hong Zhang,&nbsp;Qihao Guo,&nbsp;Benson Peter Mugaka,&nbsp;Guangjie Tai,&nbsp;Ming Xu","doi":"10.1002/cbf.70266","DOIUrl":"10.1002/cbf.70266","url":null,"abstract":"<div>\u0000 \u0000 <p>The ARHGEF (Rho guanine nucleotide exchange factor) family acts as a key upstream regulator of Rho GTPases, including RhoA, Rac1, and Cdc42. It plays critical roles in cytoskeletal remodeling, cell migration, vascular tone regulation, and inflammatory responses. Recent studies have shown that dysregulated ARHGEF activity contributes to cardiovascular diseases such as atherosclerosis, hypertension, cardiac hypertrophy, fibrosis, and myocardial ischemia/reperfusion injury. However, the functions of ARHGEFs in specific cell types and their overall signaling mechanisms in the cardiovascular system remain poorly understood. This review provides a comprehensive framework of current progress in understanding the molecular mechanisms underlying ARHGEF-mediated regulation in endothelial dysfunction, vascular remodeling, myocardial fibrosis, and ischemia/reperfusion injury. It also highlights potential pharmacological strategies that target the ARHGEF and Rho GTPase signaling axis for precise therapeutic intervention. By integrating molecular, cellular, and translational research, this work offers a conceptual framework for ARHGEF-driven signaling in cardiovascular diseases, and offers new insights for future drug development.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptotic Bodies: Decoding Their Functional Messages in Physiology and Pathology","authors":"Shanshan Xi,&nbsp;Weiran Meng,&nbsp;Xiaochi Zhu,&nbsp;Kaiwen Rao,&nbsp;Dengyi Deng,&nbsp;Qiong He,&nbsp;Pan Jin","doi":"10.1002/cbf.70260","DOIUrl":"10.1002/cbf.70260","url":null,"abstract":"<div>\u0000 \u0000 <p>Apoptosis, as the predominant form of programmed cell death, plays a crucial role in maintaining tissue homeostasis. Apoptotic bodies (ABs), which are extracellular vesicles released during the terminal phase of apoptosis, were initially characterized as functionless cellular debris. However, they are now recognized for mediating intercellular communication via biomolecule delivery in both physiological and pathological states. Owing to their diverse biological properties, ABs have emerged as promising therapeutic candidates for treating a wide range of diseases, including cancer, cardiovascular and bone diseases, neurodegenerative disorders, diabetes, and infectious/inflammatory conditions, and have demonstrated potential in promoting tissue regeneration. Furthermore, ABs present in bodily fluids carry abundant disease-related information and offer a dynamic representation of patients' physiological states, rendering them valuable tools for diagnosis and prognosis. This review consolidates progress in ABs research, delineates their pathophysiological roles, and assesses challenges and opportunities for their clinical application.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic Links Between Obesity and Breast Cancer Progression: Cellular Crosstalk, Metabolic Reprogramming and Microenvironmental Drivers","authors":"Charlise Basson,&nbsp;Michael S. Pepper,&nbsp;Anna M. Joubert,&nbsp;Melvin A. Ambele","doi":"10.1002/cbf.70263","DOIUrl":"10.1002/cbf.70263","url":null,"abstract":"<p>Obesity is increasingly recognised as an important factor contributing to cancer progression, particularly in breast cancer. However, the cellular and molecular mechanisms underlying obesity-driven breast cancer remain unclear. Several theories have been proposed to explain the complex interactions between adipose tissue and cancer, incorporating both local and distant crosstalk. This review describes existing theories on the cellular and molecular mechanisms linking obesity and breast cancer progression with a focus on inflammation, oxidative stress, metabolic reprogramming, the tumour microenvironment and crosstalk between adipose tissue and tumours. The nature of these interactions appears to be influenced by the specific characteristics of adipose tissue, including its type and anatomical location, which play distinct roles in modulating breast cancer risk and outcomes. Understanding the cellular and molecular mechanisms that underlie obesity-driven breast cancer progression may pave the way for the development of targeted therapies.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}