Chemico-Biological Interactions最新文献

{"title":"Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells","authors":"Shramana Koner,&nbsp;Seenivasan Ramasubbu","doi":"10.1016/j.cbi.2025.111868","DOIUrl":"10.1016/j.cbi.2025.111868","url":null,"abstract":"<div><div>The pervasive accumulation of plastic waste has led to widespread microplastics (MPs) pollution, raising concerns about potential human health impacts. Among these, polyethylene microplastics (PEMPs) are one of the most commonly encountered due to their prevalence in consumer products and the environment. This study investigates the cytotoxic and senescence-inducing effects of PEMPs (≤500 nm) on two cell models, A549 lung epithelial cells and Raw 264.7 macrophages. This study specifically examines cells exposed to varying concentrations of PEMPs (50–500 μg/mL), and key indicators of cellular stress were assessed, including viability, reactive oxygen species (ROS) generation, mitochondrial dysfunction, LDH release, apoptosis, and senescence. Our findings indicate that exposure to PEMPs significantly reduced cell viability and increased ROS production and mitochondrial damage in a dose- and time-dependent manner. At higher concentrations (500 μg/mL), both cell lines demonstrated that PEMPs induce apoptosis and senescence, with A549 cells showing early senescence morphology as early as 24 h post-exposure. These findings confirm the potential of PEMPs to disrupt cellular homeostasis and accelerate aging-related processes. Overall, the study reinforces the urgency of curbing plastic pollution and exploring its association with age-related pathologies and chronic health conditions.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111868"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746018","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":"Structural diversity of aldehydes determines covalent versus non-covalent inhibition mechanisms against steroid 5α-reductase type 1: Species-specific differences and preliminary structure-activity relationships","authors":"Junying Chen ,&nbsp;Shufang Qi ,&nbsp;Zijian Lin ,&nbsp;Haonan Fang ,&nbsp;Putian Zhang ,&nbsp;Wanyu Li ,&nbsp;Ren-shan Ge ,&nbsp;Yiyan Wang","doi":"10.1016/j.cbi.2025.111888","DOIUrl":"10.1016/j.cbi.2025.111888","url":null,"abstract":"<div><div>Steroid 5α-reductase type 1 (SRD5A1) plays a crucial role in neurosteroid biosynthesis, and its inhibition by environmental chemicals may disrupt brain function. This study systematically evaluated the inhibitory effects of thirteen structurally diverse aldehydes on human and rat SRD5A1 activity using microsomal enzyme assays, surface plasmon resonance (SPR) binding, cellular experiments, and computational analyses. Three aldehydes significantly inhibited human SRD5A1: o-phthalaldehyde (OPA, IC₅₀ = 2.74 μM), benzaldehyde (BEA, IC₅₀ = 45.97 μM), and cinnamaldehyde (CNA, IC₅₀ = 67.85 μM). Remarkable mechanistic differences were revealed through SPR analysis: OPA demonstrated covalent binding with incomplete dissociation (<em>K</em>_<em>D</em> = 2.16 μM), while BEA showed complete dissociation characteristic of non-covalent binding (<em>K</em>_<em>D</em> = 35.1 μM). All active compounds exhibited mixed/noncompetitive inhibition mechanisms. Species-specific differences were observed, with only OPA showing cross-species activity against rat SRD5A1. Cellular experiments revealed different potency patterns, with CNA demonstrating the strongest cellular effects despite weaker enzyme inhibition. Molecular docking revealed that OPA forms covalent bonds with Cys124 through Michael addition (−6.52 kcal/mol), while BEA and CNA rely on non-covalent interactions. DTT rescue experiments confirmed the covalent nature of OPA inhibition and the non-covalent mechanisms of BEA. OPA also uniquely affected NADPH binding kinetics, indicating its binding site spans both substrate and cofactor regions. 3D-QSAR modeling of non-covalent inhibitors identified hydrogen bond acceptor and hydrophobic features as critical for inhibition. These findings demonstrate that aldehyde structural diversity-particularly the presence of dual versus single aldehyde groups, determines both binding mechanisms and inhibitory potency, with important implications for environmental health risk assessment.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111888"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829370","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":"Copper homeostasis and its dysregulation in diseases: A focus on cuproptosis","authors":"Yixian Wang ,&nbsp;Mingyue Zhou ,&nbsp;Jin Lan ,&nbsp;Tongyao Hu ,&nbsp;Tao Wang ,&nbsp;Changjing Zuo","doi":"10.1016/j.cbi.2025.111879","DOIUrl":"10.1016/j.cbi.2025.111879","url":null,"abstract":"<div><div>Copper, an essential trace element, orchestrates diverse cellular metabolic processes through tightly regulated homeostasis. Intracellular copper homeostasis, governed by key regulators such as the copper transporter 1 (CTR1), is critical for maintaining physiological functions. Dysregulation of copper homeostasis, whether resulting in deficiency or overload, constitutes a central driver of disease pathogenesis. Notably, copper overload induces cuproptosis, a novel form of programmed cell death that has recently emerged as a promising therapeutic target across multiple diseases. Deciphering the regulatory mechanisms of cuproptosis may unlock new avenues for targeted therapy development. This review delves into the mechanisms of copper homeostasis and the pathogenic consequences of its imbalance, with a particular emphasis on cuproptosis-based strategies for cancer treatment.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111879"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752402","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":"Kalirin as a key mediator of aluminum-induced cognitive dysfunction and neurotoxicity: Integrated evidence from occupational and cellular studies","authors":"Le Zhao ,&nbsp;Jinzhu Yin ,&nbsp;Mingxing Li ,&nbsp;Yujun Ma ,&nbsp;Shihui Guo ,&nbsp;Guangsen Feng ,&nbsp;Jing Song ,&nbsp;Linping Wang ,&nbsp;Huifang Zhang ,&nbsp;Baolong Pan ,&nbsp;Xiaoting Lu","doi":"10.1016/j.cbi.2025.111853","DOIUrl":"10.1016/j.cbi.2025.111853","url":null,"abstract":"<div><div>Occupational aluminum (Al) exposure is associated with cognitive decline, but the underlying molecular mechanisms remain unclear. This study investigates the role of Kalirin in Al-induced neurotoxicity. A cross-sectional study was conducted in 2019 with 172 workers from a Shanxi aluminum plant. Participants were categorized into high and low Al exposure groups based on plasma aluminum levels, and cognitive function was assessed using the MoCA test. Phosphoproteomic analysis revealed a significant 90 % reduction in Kalirin expression in the high-exposure group compared to the low-exposure group (<em>P</em> &lt; 0.05). Multiple regression analysis demonstrated that Al exposure negatively correlated with Kalirin, GAP43, MAP2 expression, and cognitive function, while Kalirin was positively correlated with these factors (<em>q</em> &lt; 0.05). Bayesian network modeling indicated that decreased Kalirin expression, along with reduced GAP43 and MAP2 levels, increased the risk of cognitive impairment. In vitro, HT22 neurons exposed to aluminum maltolate showed reduced neuronal activity, impaired dendritic development, and disruption of the Kalirin-Rac1 pathway. Overexpression of Kalirin via lentiviral transfection reversed these effects, restoring neuronal integrity (<em>P</em> &lt; 0.05). These findings suggest that Al-induced neurotoxicity involves disruption of the Kalirin pathway, highlighting Kalirin as a potential therapeutic target for mitigating Al-related cognitive dysfunction.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111853"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145643931","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":"Subchronic co-exposure to dibutyl phthalate and benzo(a)pyrene exacerbates renal inflammation and fibrosis in rat: Crosstalk between tubular epithelial cells and fibroblasts","authors":"Jing Chen ,&nbsp;Jixing He ,&nbsp;Changzhu Long ,&nbsp;Zenglin Li ,&nbsp;Yanli Cen ,&nbsp;Yining Liu ,&nbsp;Wenyan Chen ,&nbsp;Baojun Sun ,&nbsp;Mingdan You ,&nbsp;Guanghong Yang","doi":"10.1016/j.cbi.2025.111887","DOIUrl":"10.1016/j.cbi.2025.111887","url":null,"abstract":"<div><div>Dibutyl phthalate (DBP) and benzo(a)pyrene (BaP) are commonly organic pollutants that have been simultaneously detected in environmental media, posing a significant risk to human health. However, the precise impacts and underlying mechanisms of subchronic co-exposure to DBP and BaP on the kidney remain incompletely comprehended. In this research, we evaluated the combined impact of DBP and BaP on the kidney <em>in vivo</em> and <em>in vitro</em> models. The findings exhibited that subchronic co-exposure to environmental concentrations of DBP and BaP engendered more severe inflammation and renal fibrosis than single exposure. Mechanistically, DBP and BaP co-exposure may activate the renin-angiotensin system (RAS) signaling through fibroblast growth factor 23 (FGF-23), potentially damaging renal tubular epithelial cells (RTECs). The injured RTECs further produced significant amounts of pro-inflammatory and pro-fibrotic factors, which activate surrounding fibroblasts, leading to excessive extracellular matrix (ECM) deposition and ultimately renal fibrosis. Notably, knockdown FGF-23 alleviated activation of the RAS signaling, as well as ECM production and deposition induced by DBP and BaP subchronic co-exposure. Collectively, our results indicated that DBP and BaP co-exposure may activate fibroblasts via FGF-23 activation of RAS signaling in RTECs, thereby accelerating the development of renal fibrosis.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111887"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145776513","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":"STIM1 N-linked glycosylation promotes arsenic-induced malignant phenotype by activating SOCE in bladder epithelial cells","authors":"Pinya Liu ,&nbsp;Lei Zhang ,&nbsp;Qing Zhou ,&nbsp;Zhushan Fu ,&nbsp;Shuhua Xi","doi":"10.1016/j.cbi.2025.111866","DOIUrl":"10.1016/j.cbi.2025.111866","url":null,"abstract":"<div><div>Epidemiologic research has demonstrated a clear correlation between prolonged exposure to inorganic arsenic and an elevated risk of bladder cancer, but the specific mechanisms are unknown. Calcium ions (Ca²⁺), as key second messengers, are crucial in cellular physiological and pathological processes. Loss of Ca²⁺ homeostasis is thought to be an important driver of malignant disease. In this study, C57BL/6 mice were treated with 0, 8, 20 and 50 mg/L NaAsO₂ via drinking water during 20 weeks, and human normal bladder epithelial cells (SV-HUC-1) received continuous exposure to 0.5 μM NaAsO₂ over 40 weeks. The results revealed that long-term arsenic treatment led to elevated Ca²⁺ levels in SV-HUC-1 cells and enhanced cell proliferation, stemness, and epithelial-mesenchymal transition (EMT). Our study revealed that store-operated calcium entry (SOCE) was essential in arsenic-induced elevation of Ca²⁺ levels. STIM1 serves as a critical mediator of arsenic-triggered malignant transformation in urothelial cells by regulating store-operated calcium channels (SOCC). STIM1 undergoes N-linked glycosylation at its N131 site. This post-translational modification is essential for proper STIM1 localization and binding with ORAI1. The evidence, similar to the cellular experiments in vitro, was also observed in animal experiments in vivo. Our research results provide a new mechanism for the role of calcium homeostasis imbalance in arsenic-induced initiation and progression of bladder cancer.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111866"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145727706","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":"Molecular insights into chronic glomerulonephritis and dopamine interplay","authors":"N Anirudh Singh,&nbsp;Saikat Sen","doi":"10.1016/j.cbi.2025.111880","DOIUrl":"10.1016/j.cbi.2025.111880","url":null,"abstract":"<div><div>|Glomerulonephritis (GN) is a rare kidney disorder associated with prolonged inflammation, fibrosis, and mitochondrial dysfunction at the glomeruli layer and nearby capillaries, which leads to the loss of glomeruli integrity and function. A pathogen-driven immune response is most often responsible for acute glomerulonephritis (AGN). In contrast, chronic glomerulonephritis (CGN) is more severe and characterized by irreversible loss of glomerular integrity with excessive fibrosis, often leading to progression to end-stage renal disease. Few pathways, such as WNT, Notch, PI3K/AKT, JAK-STAT, Complement, cGAS-STING, and TGF-β, have been linked to the progression and development of glomerular injury, characterized by mitochondrial dysfunction, inflammation, and fibrosis. However, the AMPK pathway has been reported to be protective against glomerular deterioration. Additionally, the dopaminergic system in the kidney has been linked to protecting glomerular integrity by downregulating mitochondrial dysfunction, inflammation, and fibrosis. This review highlights pathways that can potentially deteriorate and protect glomerular health. Additionally, it also provides an overview of the role of the dopaminergic system in attenuating glomerular injury. Suchdiscussion will provide a comprehensive understanding of potential therapeutic targets for attenuating CGN.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111880"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752411","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":"Pachymic acid suppresses proliferation and invasion in colon cancer by inhibiting glycolysis via PPARγ/ENO1 pathway","authors":"Zhiwei Wang ,&nbsp;Peiyao Wu ,&nbsp;Chuanzhuo Zhang ,&nbsp;Ting Zhang ,&nbsp;Chunlin Gu ,&nbsp;Xiaodong Xie ,&nbsp;Xiao Feng ,&nbsp;Zhiwei Jiang","doi":"10.1016/j.cbi.2025.111881","DOIUrl":"10.1016/j.cbi.2025.111881","url":null,"abstract":"<div><div>Aerobic glycolysis constitutes a fundamental aspect of the process of tumor development. Pachymic acid, a major active ingredient in <em>Poria cocos</em>, has been reported to impair glucose metabolism in several cancers. However, whether pachymic acid could inhibit the aerobic glycolysis of colon cancer remains to be elucidated. Our study revealed that the treatment of pachymic acid significantly inhibited the proliferation and invasion of HT-29 and HCT-116 cells. Moreover, it led to a substantial reduction in the expression level of glycolysis-related proteins including phosphoglycerate kinase 1 (PGK1), glucose transporter 1 (GLUT1), lactate dehydrogenase A (LDHA) and α-enolase (ENO1). Potential targets of pachymic acid were screened by network pharmacology analysis and molecular docking, and PPARγ was determined as the primary target of pachymic acid according to Western blot and real-time qPCR. Further experiments indicated that the overexpression of PPARγ reversed the inhibitory effects of pachymic acid on the proliferation, invasion and aerobic glycolysis of HT-29 and HCT-116 cells. The inhibition of PPARγ led to a significant reduction in the expression of PGK1, GLUT1, LDHA and ENO1. Subcutaneous tumor-bearing experiments in nude mice verified the antitumor effect of pachymic acid on colon cancer, which could be reversed by the overexpression of PPARγ. The present study confirmed that pachymic acid played an inhibitory role in the proliferation and invasion of colon cancer by intervening in the process of glycolysis. PPARγ was identified as the primary target of pachymic acid in regulating the glucose metabolism in colon cancer.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111881"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752428","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":"Embracing dishonesty: How LNT became king","authors":"Edward J. Calabrese,&nbsp;Paul B. Selby","doi":"10.1016/j.cbi.2025.111832","DOIUrl":"10.1016/j.cbi.2025.111832","url":null,"abstract":"<div><div>The US NAS BEAR I Genetics Panel in 1956 offered a profoundly influential recommendation to switch from a threshold to a linear dose response model for radiation-induced hereditary changes and key gene-mutation-mediated somatic endpoints. Historical and recent findings indicate that this NAS Report is based on falsified data from panelist William L. Russell that significantly inflated panelist estimates of radiation-induced mutational risks and that panelist James Crow disguised massive panelist uncertainty and variability to promote acceptance of its LNT-risk-based recommendations. This paper extends those challenges to the integrity and credibility of the 1956 NAS report and of decisions by regulatory agencies such as the US EPA to adopt such recommendations by showing that: (1) the “esteemed” NAS panel lacked the necessary expertise to guide the country on radiation-induced genetic risks based on a strikingly anemic research publication record on that topic, (2) selection of the panelists was influenced by commitments toward an evolutionary-based eugenics framework, (3) a key eugenics strategy involved the adoption of an LNT model for risk assessment to reduce population genetic variability, and (4) Muller persuaded the Panel chair to add Crow to blunt an anticipated challenge to Muller's genetic load hypothesis by population geneticists based on enhanced fitness in heterozygotes at optimized radiation exposures, which challenged his eugenics framework. In addition, the selection of a Panel scientifically weak regarding radiation experiments may have been intentional to allow Muller to dominate Panel activities consistent with his eugenics perspectives. It appears likely that Muller and Crow conspired to manipulate Panel activities, leading to the adoption of LNT for radiation risk assessment, as part of the larger RF plan to control the direction of human evolution via eugenics principles and practices.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111832"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673060","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":"The ADME profile of threo-4-methylmethylphenidate (4-Mmph, 4-MeTMP, CAS: 467468-40-2) as new psychoactive substance (NPS): Prediction of absorption, distribution, metabolism and excretion parameters using integrated in silico approach for clinical and forensic purposes","authors":"Łukasz Niżnik ,&nbsp;Kamil Jurowski","doi":"10.1016/j.cbi.2025.111861","DOIUrl":"10.1016/j.cbi.2025.111861","url":null,"abstract":"<div><div>Threo-4-methylmethylphenidate (4-Mmph, 4-MeTMP, CAS: 467468-40-2) is a stimulant that could be recognized as a new psychoactive substance. It is a derivative of methylphenidate, which is a medicament for treating attention deficit hyperactivity disorder. This study aims to use integrated <em>in silico</em> methods to predict the absorption, distribution, metabolism, and excretion (ADME) of 4-Mmph for the first time. The absorption potential of 4-Mmph indicates gastrointestinal absorption and potential brain penetration, however that it is neither a substrate nor an inhibitor of P-glycoprotein. The predictions of water solubility show a range of estimates, all indicating high gastrointestinal absorption. However, the Caco-2 permeability data are inconsistent between the methods, necessitating further experimental validation. Metabolism predictions focus on interactions with CYP450 enzymes, showing varied results across different tools. Consistent predictions are seen for CYP2C19 and CYP2C9, with low substrate and inhibitor activity. The predictions of CYP2D6 and CYP3A4 show discrepancies, highlighting the importance of using multiple tools for a complete metabolic profile. Potential phase I and phase II reactions are also indicated within this study. 4-Mmph is not identified as a substrate for the renal organic cation transporter OCT2, implying alternative renal excretion pathways.</div></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"424 ","pages":"Article 111861"},"PeriodicalIF":5.4,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682633","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}