Environment & Health
·
2026
·
IF 8.8
Yueyue Mu,Jiawei Wu,Xiaomeng Ding,Yanting Pang,Yuna Cao,Jing Qu,Haopeng Zhang,Qing Liu,Ting Zhang
Indium tin oxide (ITO) particles, widely utilized in electronics and energy technologies, pose significant pulmonary risks due to occupational exposure during manufacturing. While emerging evidence links ITO to severe lung pathologies, critical gaps persist in understanding size-dependent effects and molecular mechanisms. This study systematically investigates the size-dependent effects of nanoscale ITO (N-ITO) and submicron-scale ITO (U-ITO) on pulmonary toxicity, focusing on ferroptosis as a key mechanism. In vivo, repeated oropharyngeal exposure of mice to ITO (3.6 and 36 mg/kg) induced dose-dependent lung inflammation and ferroptosis, marked by lipid peroxidation, Fe2+ accumulation, and dysregulation of Gpx4 and Scl7a11 proteins, with pulmonary macrophages identified as primary targets. In vitro, THP-1 macrophages exposed to 6.25–25 μg/mL ITO exhibited size-dependent cytotoxicity, inflammation, and ferroptotic hallmarks. Mechanistically, ITO-triggered ferroptosis promoted HMGB1 secretion and nuclear translocation, which activated the RAGE/p38MAPK pathway, amplifying inflammatory responses. Notably, N-ITO induced stronger ferroptosis and inflammation than U-ITO, correlating with enhanced macrophage uptake due to its nanoscale dimensions. Integrating these findings, we propose an Adverse Outcome Pathway (AOP) framework for ITO-induced lung injury, which cellular uptake may serve as the molecular initiating event and link ferroptosis-driven high mobility group protein B1 (HMGB1) release, RAGE/p38MAPK activation, and chronic inflammation to adverse pulmonary outcomes. This study underscores the necessity of size-specific occupational exposure limits for ITO nanoparticles and provides a mechanistic foundation for risk assessment and management strategies in occupational settings.
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DOI
高影响因子
Molecular Medicine Reports
·
2022
·Vol. 26
·期 6
·1-11
·
IF 3.423
Wenjuan Guo,Xiaodi Wang,Fang Liu,Shuo Chen,Shuai Wang,Qingrui Zhang,Lan Yuan,Shiyu Du
Ulcerative colitis (UC) is a significant burden on human health, and the elucidation of the mechanism by which it develops has potential for the prevention and treatment of UC. It has been reported that acteoside (ACT) exhibits strong anti‑inflammatory activity. In the present study, it was hypothesized that ACT may exert a protective effect against UC. The effects of ACT on inflammation, oxidative stress and apoptosis were evaluated using dextran sulphate sodium (DSS)‑treated mice and DSS‑treated human colorectal adenocarcinoma Caco‑2 cells, which have an epithelial morphology. The results demonstrated that the ACT‑treated mice with DSS‑induced UC exhibited significantly reduced colon inflammation, as demonstrated by a reversal in body weight loss, colon shortening, disease activity index score, inflammation, oxidative stress and colonic barrier dysfunction. Further in vivo experiments demonstrated that ACT inhibited DSS‑induced apoptosis in colon tissues, as demonstrated by the results of the TUNEL assay and the altered protein expression levels of Bax, cleaved caspase‑3 and Bcl‑2. Furthermore, DSS significantly stimulated the protein expression levels of high mobility group box 1 protein (HMGB1), which serves a central role in the initiation and progression of UC, an effect which was markedly inhibited by ACT. Finally, DSS significantly decreased the protein expression levels of heme oxygenase‑1 (HO‑1) in colon tissues and the effect of ACT on GSH, apoptotic proteins and HMGB1 was markedly attenuated in the presence of the HO‑1 inhibitor tin protoporphyrin. In conclusion, ACT ameliorated colon inflammation through HMGB1 inhibition in a HO‑1‑dependent manner.
研究领域:
药理学
·
免疫学
·
胃肠病学
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DOI
PubMed
高影响因子
Antioxidants
·
2024
·Vol. 13
·期 7
·803
·
IF 6
Zhen Shen,Yun-Dan Guo,Ming-Ze Tang,Ping Zhou,Yu-Xin Su,Hao-Ran Shen,Tao Li,Wei Jiang,Yan-Xing Han,Cai Tie,Jing-Jing Cui,Tian-Le Gao,Jian-Dong Jiang
Pregabalin is a medication primarily used in the treatment of neuropathic pain and anxiety disorders, owing to its gabapentinoid properties. Pregabalin monotherapy faces limitations due to its variable efficacy and dose-dependent adverse reactions. In this study, we conducted a comprehensive investigation into the potentiation of pregabalin’s analgesic effects by dexborneol, a neuroprotective bicyclic monoterpenoid compound. We performed animal experiments where pain models were induced using two methods: peripheral nerve injury, involving axotomy and ligation of the tibial and common peroneal nerves, and incisional pain through a longitudinal incision in the hind paw, while employing a multifaceted methodology that integrates behavioral pharmacology, molecular biology, neuromorphology, and lipidomics to delve into the mechanisms behind this potentiation. Dexborneol was found to enhance pregabalin’s efficacy by promoting its transportation to the central nervous system, disrupting self-amplifying vicious cycles via the reduction of HMGB1 and ATP release, and exerting significant anti-oxidative effects through modulation of central lipid metabolism. This combination therapy not only boosted pregabalin’s analgesic property but also notably decreased its side effects. Moreover, this therapeutic cocktail exceeded basic pain relief, effectively reducing neuroinflammation and glial cell activation—key factors contributing to persistent and chronic pain. This study paves the way for more tolerable and effective analgesic options, highlighting the potential of dexborneol as an adjuvant to pregabalin therapy.
研究领域:
药理学
·
神经科学
·
分子生物学
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DOI
PubMed
高影响因子
CURRENT PHARMACEUTICAL BIOTECHNOLOGY
·
2021
·Vol. 22
·期 12
·1672-1682
·
IF 2.837
Qiu Chengjiang,Liu Kairui,Li Xuguang,Chen Weirun,Zhang Sheng,Huang Youxing
Background: The pathogenesis of Severe Acute Pancreatitis (SAP) is mediated substantially by dysfunctions in the intestinal barrier. Euphorbia kansui (EK) is a medicinal plant used widely in traditional Chinese medicine to treat inflammation; however, its efficacy and mechanism of action
in SAP treatment are not yet well understood. Objective: To investigate the role of EK in intestinal barrier tissue repair and in the pathogenesis and development of SAP. Methods: The rat SAP model was established by a retrograde injection of sodium taurocholate into the pancreatic
bile duct. The SAP model group and the SAP + EK treatment groups were divided into 6 subgroups according to timing: 2, 6, 12, 24, 48, or 72h after inducing SAP. The progression of the SAP rats and of the rats receiving the EK treatment was evaluated using the ascites volume, serum amylase
and plasma endotoxin levels, and histological grading of intestinal mucosal damage. In addition, serum inflammatory factor contents were measured using Enzyme-Linked Immunosorbent Assay (ELISA) tests and apoptotic cells in damaged ileum tissue were detected using TUNEL staining. Apoptosis
markers and other signaling proteins in intestinal mucosal cells were detected by immunohistochemical assays and then validated by combining these data with quantitative polymerase chain reactions and western blotting. Results: Compared with the results of the SAP model rats, the results
of the rats that received EK treatment demonstrated that EK could effectively reduce the ascites volume and serum amylase and plasma endotoxin levels. EK treatment also greatly reduced the abnormal intestinal morphological alterations in the rat SAP model and significantly downregulated the
serum contents of Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. EK treatment inhibited the elevation of capapse-3, inhibited the decrease of the Bcl-2 protein, and decreased the number of apoptotic cells in rat ileum tissue. Finally, EK treatment abrogated the increase
of HMGB1 and the suppression of MFG-E8 protein expression in the SAP + EK rat ileum tissue. Conclusion: EK suppresses SAP pathogenesis by restoring the intestinal barrier function and modulating the HMGB1/MFG-E8 signaling axis.
研究领域:
药理学
·
病理生理学
·
中医药学
·
分子生物学
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2021
·
IF 4.432
Jing-Mei Lu,Guang-Nan Jin,Yu-Nan Lu,Xu-Dong Zhao,Hui-Wen Lan,Shuai-Ru Mu,Xin-Yu Shen,Guang-Hua Xu,Cheng-Hua Jin,Juan Ma,Xuejun Jin,Xiang Xu,Lian-Xun Piao
Toxoplasma gondii ( T. gondii ) is an obligate intracellular parasite that can cause liver diseases in the host, including hepatitis and hepatomegaly . High mobility group box 1 (HMGB1) is the main inflammatory mediator causing cell injury or necrosis. HMGB1 binds to toll like receptor 4 (TLR4), then activates the nuclear factor-κB (NF-κB) signaling pathway, which promotes the release of inflammatory factors. Our previous studies showed that HMGB1 mediated TLR4/NF-κB signaling pathway plays an important role in liver injury induced by T. gondii infection. Resveratrol (RSV) is a small polyphenol, which has anti-inflammatory, anti-cancer, anti- T. gondii effect. However, the effect of RSV on liver injury caused by T. gondii infection is unclear. This study used the RH strain tachyzoites of T. gondii to infect murine liver line, NCTC-1469 cells to establish an in vitro model and acute infection of mice for the in vivo model to explore the protective effect of RSV on liver injury induced by T. gondii infection. The results showed that RSV inhibited the proliferation of T. gondii in the liver, reduced the alanine aminotransferase/aspartate aminotransferase levels and pathological liver damage. Additionally, RSV inhibited the production of tumor necrosis factor-α, inducible nitric oxide synthase and HMGB1 by interfering with the TLR4/NF-κB signaling pathway. These results indicate that RSV can protect liver injury caused by T. gondii infection by intervening in the HMGB1/TLR4/NF-κB signaling pathway. This study will provide a theoretical basis for RSV treatment of T. gondii infection induced liver injury.
研究领域:
免疫学
·
药理学
·
寄生虫学
·
分子生物学
·
病理学
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DOI
PubMed
高影响因子
ANALYTICA CHIMICA ACTA
·
2025
·
IF 6
Hong Zhang,Xuekun Bai,Chenxi Wang,Wei Pang,Jiaxin Zhang,Junhuai Song,Huanying Zhou,Zhixian Gao,Bin Zheng
Background Biorhythmic played an important role in physical health. Biorhythmic disorders led to various health issue, including cardiovascular diseases and metabolic disorders. Early diagnosis of biorhythmic disorders was crucial in slowing the progression of disease. Therefore, it was important to develop technologies for detecting biorhythmic and their disorder markers. This study selected HMGB1(High mobility group box 1), BMAL1 (Brain and Muscle Aryl hydrocarbon receptor nuclear translocator-like 1), and MICU (mitochondrial calcium uptake 1) mRNA for detection. Results CRISPR/Cas12a/SERS (surface-enhanced Raman spectroscopy) ultrasensitive biosensing platform was developed for the detection of biorhythmic markers. The biosensor was partly an ultrabright Raman signal reporter (on) of a novel satellite structure formed by gold/silver bimetallic nanoparticles. This novel satellite structure utilizes the potential difference between gold and silver nanoparticles to promote the transfer of electrons from the core structure to the AuNPs and MBA (4-mercaptobenzoic acid) molecules, while enhancing the electromagnetic field distribution. Compared with the Raman signal of the satellite structure composed of Au/Au bimetallic, the Raman signal of the satellite structure in this study is increased by about 10 times. CRISPR/Cas12a recognized the target molecule and activated trans -cleavage activity, cleaving the DNA/RNA hairpin structure and releasing RNA 2∗ . RNA 2∗ caused the satellite structure to disperse, significantly attenuating the ultra-strong Raman signal (off), thereby enabling quantitative detection of the target nucleic acid. The LOD for three targets were of less than 1 fM. Significance In summary, the CRISPR/Cas12a/SERS biosensing platform enables mRNA detection without preamplification. This biosensing platform can detect target molecules at the fM level, achieving ultra-sensitive detection. In addition, the satellite structure exhibits long-term stability, providing a theoretical basis for the practical application of this biosensing platform.
研究领域:
生物传感器
·
分子诊断学
·
纳米技术
·
CRISPR技术
·
RNA检测
·
生物医学工程
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产品关联
DOI
PubMed
高影响因子
Autophagy
·
2018
·
IF 11.1
Peihua Luo,Zhifei Xu,Guanqun Li,Hao Yan,Yi Zhu,Hong Zhu,Shenglin Ma,Bo Yang,Qiaojun He
Sunitinib, a multikinase inhibitor approved for a number of cancer indications has a low response rate. Identifying mechanisms of resistance could lead to rational combination regimens that could improve clinical outcomes. Here we report that resistance to sunitinib therapy was driven by autophagic degradation of TP53/p53. Deletion of ATG7 or ATG5 suppressed TP53 degradation, as did knockdown of SQSTM1/p62. Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs). Moreover, TP53 degradation was achieved by the transport of its nuclear binding target, HMGB1, which shifted TP53 from the nucleus to the cytoplasm. The inhibition of HMGB1 sensitized cancer cells to sunitinib. Importantly, sunitinib induced the degradation of all TP53 proteins, except for TP53 proteins with mutations in the interaction domain of TP53 with HMGB1 (amino acids 313 to 352). In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.
研究领域:
肿瘤学
·
分子生物学
·
癌症治疗
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DOI
PubMed
高影响因子
JOURNAL OF SEPARATION SCIENCE
·
2026
·Vol. 49
·期 4
·e70402
·
IF 3.6
Xinlin Chen,Junxi Liu,Liping Qu,Feifei Wang
High Mobility Group Box 1 (HMGB1), a non-histone chromatin protein, is a key inflammatory cytokine. Direct HMGB1 inhibitors have gained attention for their therapeutic potential in age-related diseases by blocking the pro-inflammatory activity of extracellular HMGB1, but remain limited. Here, an immobilized HMGB1 was synthesized in one step using an oriented immobilization approach and applied to efficiently acquire direct HMGB1 inhibitors from a highly complex matrix. The oriented immobilization method employed a Ni 2 + -modified metal–organic framework combined with cell lysate containing engineered His-tagged HMGB1, bypassing the need for pre-purified proteins. The resulting immobilized HMGB1 demonstrated high protein loading capacity (110.2 mg/g) while retaining its cytokine activity. The immobilized HMGB1 was employed to rapidly identify its direct inhibitors from the Taxus wallichiana var. mairei twig. The application of this immobilized HMGB1 enabled efficient capture of 11 HMGB1 ligands from this plant. Among the 11 ligands, seven compounds were structurally characterized by HPLC-Q-TOF-MS/MS. Among these compounds, sciadopitysin was selected due to its higher HMGB1 inhibitory activity and predicted binding affinity to HMGB1. Through fluorescence quenching and surface plasmon resonance analyses, sciadopitysin was experimentally validated, where the surface plasmon resonance data demonstrated direct binding to HMGB1 with a dissociation constant (K d ) of 2.77 × 10 −4 M, and the observed intrinsic fluorescence quenching provided additional evidence of the ligand–protein interaction. Furthermore, validation in RAW264.7 macrophages demonstrated its dose-dependent suppression of HMGB1-stimulated inflammation (IC 50 = 27.25 ± 3.31 µM). Collectively, a highly efficient ligand fishing strategy for identifying direct HMGB1 inhibitors was established. Moreover, our findings illustrated the correlation between Taxus wallichiana var. mairei and HMGB1 inhibition.
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产品关联
DOI
PubMed
高影响因子
Chinese Journal of Natural Medicines
·
2024
·
IF 4
Wenhui YAO,Rongpin TAO,Kai WANG,Xuansheng DING
ABSTRACT Icariin, a flavonoid glycoside, is extracted from Epimedium . This study aimed to investigate the vascular protective effects of icariin in type 1 diabetic rats by inhibiting high-mobility group box 1 (HMGB1)-related inflammation and exploring its potential mechanisms. The impact of icariin on vascular dysfunction was assessed in streptozotocin (STZ)-induced diabetic rats through vascular reactivity studies. Western blotting and immunofluorescence assays were performed to measure the expressions of target proteins. The release of HMGB1 and pro-inflammation cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The results revealed that icariin administration enhanced acetylcholine-induced vasodilation in the aortas of diabetic rats. It also notably reduced the release of pro-inflammatory cytokines, including interleukin-8 (IL-8), IL-6, IL-1β, and tumor necrosis factor-alpha (TNF-α) in diabetic rats and high glucose (HG)-induced human umbilical vein endothelial cells (HUVECs). The results also unveiled that the pro-inflammatory cytokines in the culture medium of HUVECs could be increased by rHMGB1. The increased release of HMGB1 and upregulated expressions of HMGB1-related inflammatory factors, including advanced glycation end products (RAGE), Toll-like receptor 4 (TLR4), and phosphorylated p65 (p-p65) in diabetic rats and HG-induced HUVECs, were remarkably suppressed by icariin. Notably, HMGB1 translocation from the nucleus to the cytoplasm in HUVECs under HG was inhibited by icariin. Meanwhile, icariin could activate G protein-coupled estrogen receptor (GPER) and sirt1. To explore the role of GPER and Sirt1 in the inhibitory effect of icariin on HMGB1 release and HMGB-induced inflammation, GPER inhibitor and Sirt1 inhibitor were used in this study. These inhibitors diminished the effects of icariin on HMGB1 release and HMGB1-induced inflammation. Specifically, the GPER inhibitor also negated the activation of Sirt1 by icariin. These findings suggest that icariin activates GPER and increases the expression of Sirt1, which in turn reduces HMGB1 translocation and release, thereby improving vascular endothelial function in type 1 diabetic rats by inhibiting inflammation.
研究领域:
药理学
·
内分泌学
·
心血管疾病
·
分子生物学
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DOI
高影响因子
Journal of Translational Medicine
·
2026
·Vol. 24
·期 1
·539
·
IF 9.7
Gao Yuan-Yuan,Sun Wen-Shuang,Sun Zi-Ying,Wang Jun-Rui,Lv Zhong-Yang,Li Yu-Jia,Tian Hao-Yuan,Bao Zheng-Yang,Qiu Xin-Ran,Wang Zheng,Zheng Shi-Zhong,Shao Jiang-Juan,Zhang Zi-Li,Meng Jia
Background Tendinopathy is a prevalent orthopaedic condition characterized by disrupted tendon homeostasis, with oxidative stress being a key contributing mechanism. Although the natural compound 18-β-Glycyrrhetinic acid (GA) exhibits antioxidant properties and is a therapeutic candidate for tendinopathy, its precise molecular mechanism remains unclear. This study aimed to elucidate how GA alleviates tendinopathy, with a focus on its role in regulating the HMGB1-cGAS-STING axis and NLRP3 inflammasome activation in the context of oxidative stress. Methods We employed single-cell RNA sequencing (scRNA-seq) of clinical samples, proteomics of animal tissues, and comprehensive pharmacological assays to investigate the mechanisms of tendinopathy. Furthermore, the rat tendinopathy model and H 2 O 2 -induced oxidative stress model of tendon stem cells (TSCs) were used to validate the protective effects of GA. Results We found that GA significantly reduced oxidative stress and subsequent inflammation, thereby mitigating collagen disruption in rats with tendinopathy. Notably, scRNA-seq revealed that the proportion of TSCs increased significantly during tendinopathy, which were particularly susceptible to reactive oxygen species (ROS). TSCs from oxidative damage and inhibited activation of the NLRP3 inflammasome by suppressing the cGAS-STING pathway. Mechanistically, GA promoted cGAS degradation by enhancing its interaction with the mitochondrial E3 ubiquitin ligase Mul1. This effect was mediated through high-mobility group box 1 (HMGB1), as GA disrupted the HMGB1-cGAS interaction. Specifically, GA induced methylation of HMGB1 at lysine 43, a modification essential for its activity. This methylation was catalyzed by the methyltransferase DOT1L, which was upregulated and directly bound by GA. Collectively, GA alleviates tendinopathy by targeting the DOT1L-HMGB1-cGAS axis to resolve oxidative stress and inflammation. Conclusion Collectively, our findings provide new insights into how oxidative stress accelerates tendinopathy progression. Moreover, they delineate the mechanism by which GA in mitigates oxidative damage and inflammation in TSCs by inhibiting the co-localization of HMGB1 and cGAS. Overall, this study offers scientific support for further developing GA as a promising therapeutic agent for tendinopathy treatment. Graphical The alternative text for this image may have been generated using AI.
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高影响因子
ACTA PHARMACOLOGICA SINICA
·
2025
·
IF 8.4
Ye Cui-fang,Wu Jia-di,Li Lin-rong,Sun Shu-guo,Wang Yu-gang,Jiang Tian-an,Long Xin,Zhao Jun
Irreversible electroporation (IRE) is a local ablative treatment for patients with pancreatic cancer. During the IRE procedure, high-intensity electric pulses are released intratumorally to disrupt plasma membranes and induce cell death. Since the intensity of the pulsed electric field (PEF) can be decreased by the tumor microenvironment, some cancer cells are subjected to a sublethal PEF and may survive to cause tumor recurrence later. Autophagy activation induced by anticancer therapies is known to promote treatment resistance. In this study, we investigated whether autophagy is activated in residual cancer cells after IRE and assessed the roles it plays during tumor recurrence. Subcutaneous KPC-A548 or Panc02 murine pancreatic cancer cell line xenograft mouse models were established; once the tumors reached 7 mm in one dimension, the tumor-bearing mice were subjected to IRE. For in vitro sublethal PEF treatment, the pancreatic cancer cell suspension was in direct contact with the electrodes and pulsed at room temperature. We showed that autophagy was activated in surviving residual cells, as evidenced by increased expression of LC3 and p62. Suppression of autophagy with hydroxychloroquine (60 mg/kg, daily intraperitoneal injection) markedly increased the efficacy of IRE. We demonstrated that autophagy activation can be attributed to increased expression of high-mobility group box 1 (HMGB1); co-inhibition of two HMGB1 receptors, receptor for advanced glycosylation end products (RAGE) and Toll-like receptor 4 (TLR4), suppressed autophagy activation by upregulating the PI3K/AKT/p70 ribosomal S6 protein kinase (p70S6K) axis and sensitized pancreatic cancer cells to PEF. We prepared a polymeric micelle formulation (M-R/T) encapsulating inhibitors of both RAGE and TLR4. The combination of IRE and M-R/T (equivalent to RAGE inhibitor at 10.4 mg/kg and TLR4 inhibitor at 5.7 mg/kg, intravenous or intraperitoneal injection every other day) significantly promoted tumor apoptosis, suppressed cell cycle progression, and prolonged animal survival in pancreatic tumor models. This study suggests that disruption of HMGB1-mediated autophagy with nanomedicine is a promising strategy to enhance the response of pancreatic cancer to IRE.
研究领域:
肿瘤学
·
癌症生物学
·
分子生物学
·
药理学
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DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2026
·
IF 7.2
Zixu Li,Muge Xu,Yahan Zhang,Yao Chen,Weiwei Feng,Ting Zhao,Liuqing Yang,Guanghua Mao,Xiangyang Wu
The widespread presence of plastic pollutants, particularly phthalate esters such as dibutyl phthalate (DBP), poses a significant threat to both ecosystems and human health. Despite the accumulating evidence of DBP toxicity, the mechanisms driving DBP-induced hepatotoxicity remain poorly understood. In this study, an integrated approach combining network toxicology, molecular docking, and multidimensional experimental validation was applied to elucidate the molecular pathways through which DBP causes liver damage. Ferroptosis was identified as a central player in DBP-induced hepatotoxicity. The results showed that DBP activates the aryl hydrocarbon receptor (AhR), regulating the NRF2/HO-1 signaling axis, which in turn induces iron overload and lipid peroxidation. Furthermore, ferroptotic hepatocytes release high-mobility group box 1 (HMGB1), activating the TLR4/NF-κB pathway in macrophages and amplifying inflammatory responses that exacerbate liver injury. Crucially, inhibition of either AhR expression or ferroptosis significantly attenuated these changes, highlighting the potential of AhR and ferroptosis as therapeutic targets. Together, these findings establish a novel mechanistic framework for DBP-induced hepatotoxicity: the AhR–NRF2/HO-1–ferroptosis–HMGB1/TLR4 axis. This study advances our understanding of plasticizer toxicity and offers insights for risk assessment and intervention strategies for combating environmental hepatotoxins.
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PubMed
高影响因子
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