FASEB JOURNAL
·
2026
·Vol. 40
·期 14
·e72154
·
IF 4.3
Ya‐Ping Li,Fei‐Hong Huang,Meng‐Ting Wu,Meng‐Yi Chen,Yong‐Ping Wen,Xiang Li,Lu Yu,An‐Guo Wu,Jian‐Ming Wu,Xiao‐Gang Zhou
Ferroptosis contributes to aging‐associated functional decline, yet compounds with robust organismal efficacy and defined upstream regulatory mechanisms remain limited. Here, we established a diethyl maleate (DEM)‐induced glutathione depletion model in wild‐type (N2) Caenorhabditis elegans as a survival‐based screening platform and identified syringaresinol (Syr) as a leading hit from an in‐house small‐molecule library. In nematodes, Syr improved survival under DEM challenge, reduced lipid peroxidation, reactive oxygen species (ROS), and malondialdehyde levels, and alleviated age‐associated oxidative lipid stress and iron imbalance during natural aging, accompanied by extended lifespan and improved healthspan‐related phenotypes. In primary human foreskin fibroblasts, Syr conferred dose‐dependent protection against RSL3‐ or erastin‐induced ferroptosis, preserved cellular integrity, suppressed lipid peroxidation and ROS, and restored expression of GPX4, SLC7A11, and ferritin. In two senescence models, Syr also attenuated senescence‐associated phenotypes and ferroptosis‐related oxidative lipid stress, concomitant with recovery of GPX4 expression. Network‐based prediction and functional perturbation identified HIF‐1α as a candidate mediator of Syr‐associated cytoprotection. HIF‐1α knockdown weakened Syr‐mediated protection and largely prevented GPX4 restoration, whereas GPX4 knockdown did not alter HIF‐1α abundance. These findings support a functional HIF‐1α–GPX4 defense axis in fibroblasts, while direct transcriptional regulation remains to be clarified. Overall, Syr attenuates ferroptosis‐relevant oxidative lipid stress and aging‐associated phenotypes in C. elegans and human fibroblast models, supporting further mechanistic and mammalian in vivo validation. A 220‐compound screen in DEM‐challenged C. elegans identified syringaresinol (Syr) as a lead protective compound. Syr alleviated aging‐ and ferroptosis‐associated phenotypes in C. elegans and human foreskin fibroblasts by reducing lipid peroxidation, ROS accumulation, MDA levels, labile Fe 2+ , cell death, and SA‐β‐gal activity, while restoring GPX4/SLC7A11/ferritin‐associated defense responses. The proposed mechanism suggests that Syr attenuates senescence‐associated functional decline through a HIF‐1α‐associated GPX4 protective axis. The dashed arrow denotes a hypothesized mediator or interaction that remains to be experimentally validated.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CYTOKINE
·
2023
·
IF 3.8
Wei Liu,Hui Zeng
Background Ulcerative colitis (UC) is a chronic and uncontrolled inflammatory bowel disease. N 6 -methyladenine (m 6 A) is a reversible mRNA modification method. IGF2BP2 is an RNA-binding protein regulated by m 6 A methylation. However, understanding of m 6 A-related proteins in UC is limited. This study was to analyze the function and related mechanism of IGF2BP2 in UC. Methods The UC models were established by dextran sulfate sodium (DSS) in NCM460 cells and mice. The expression of IGF2BP2 and GPX4 in UC were detected by qPCR and western blot. The effects of IGF2BP2 on inflammation, ferroptosis and colon injury were measured by gain- and loss-of-function experiments. This study conducted a clinical evaluation of mice using the Disease Activity Index score. The molecular mechanism of IGF2BP2 in ferroptosis were analyzed by m 6 A RNA methylation quantification kit, RNA immunoprecipitation-qPCR analysis, and RNA stability assay. Results IGF2BP2 and GPX4 were under-expressed in DSS-treated UC. IGF2BP2 enhanced the stability of GPX4 mRNA modified by m 6 A. IGF2BP2 overexpression repressed the ROS, MDA, and iron levels but enhanced the GSH and GPX4 levels in DSS-triggered NCM460 cells, which were partially reversed by GPX4 silencing. In UC mice, IGF2BP2 high-expression ameliorated symptoms, Disease Activity Index score, pathological changes, inflammatory reaction, and ferroptosis, which were also partly neutralized by GPX4 inhibition. Conclusions IGF2BP2 augmented the GPX4 expression by the m 6 A modification to weaken UC progression via suppressing ferroptosis.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Materials Today Bio
·
2026
·
IF 11
Xueping Luo,Yixin Liu,Guangmiao Chen,Xinrui Ma,Pingping Xu,Yutong Li,Longyu Zheng,Rongrong Zheng,Youqin Xu,Shiying Li,Linping Zhao
Ferroptosis, a form of regulated cell death that is iron-dependent and driven by the accumulation of lipid peroxides (LPO), has emerged as a promising avenue for enhancing tumor immunogenicity and augmenting immune checkpoint blockade (ICB) efficacy. In this study, we demonstrated that dBET57, a BRD4-targeting PROTAC, potently suppresses the expression of GPX4, the master negative regulator of ferroptosis, thereby triggering ferroptotic cell death, while concurrently downregulating PD-L1 to reverse immune evasion. Based on this, we developed a self-assembled nano-PROTAC platform, termed dBET@TF, designed to amplify ferroptosis and potentiate colorectal cancer immunotherapy. Specifically, dBET@TF was constructed via self-assembly of dBET57, tannic acid, and Fe 3+ , which endowed the formulation with acid-responsive drug release capability and significantly improved its intracellular delivery efficiency. Mechanistically, dBET@TF promoted ferroptosis through iron accumulation and GPX4 depletion, triggering robust immunogenic cell death (ICD). Concurrently, BRD4 degradation mediated by dBET@TF durably suppressed PD-L1 expression, reprogramming the tumor microenvironment to foster enhanced immune activation, characterized by increased infiltration of natural killer (NK) cells and cytotoxic T lymphocytes (CTLs). As a result, dBET@TF significantly potentiated the therapeutic response to αPD-1 in both primary tumor and experimental lung metastasis models. Overall, this work establishes a novel PROTAC-based therapeutic strategy that leverages BRD4 degradation to amplify ferroptosis and remodel antitumor immunity, offering a promising approach to potentiate colorectal cancer immunotherapy.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Bioscience-Landmark
·
2026
·Vol. 31
·期 7
·
IF 4.1
Zhenxin Huo,Ding Li,Yuxuan Kuang,Baoshan Xu
Background: Intervertebral disc degeneration (IDD) is a major pathological contributor to low back pain, and its progression is closely associated with oxidative stress and cell death. Ferroptosis is a form of programmed cell death characterized by iron-dependent lipid peroxidation, which has recently been confirmed to participate in IDD progression. Microsomal glutathione S-transferase 1 (MGST1) plays an important role in glutathione metabolism and cellular antioxidant defense, but its function in IDD remains unclear. This study aimed to investigate the expression profile of MGST1 in IDD and to elucidate its molecular mechanism in delaying degeneration by regulating ferroptosis. Methods: Differentially expressed ferroptosis-related genes associated with intervertebral disc degeneration were screened through bioinformatics analysis. MGST1 expression changes were validated using a needle puncture-induced rat IDD model and a degenerated nucleus pulposus (NP) cell model. MGST1 knockdown and overexpression strategies were employed to evaluate its effects on the extracellular matrix metabolism, apoptosis, and senescence of nucleus pulposus cells. Further examinations of ferroptosis-related indicators were conducted, including levels of lipid peroxidation, reactive oxygen species generation, intracellular Fe2+ content, and changes in mitochondrial membrane potential. For in vivo experiments, the therapeutic effect of MGST1 overexpression was assessed by intradiscal injection of an MGST1-overexpressing lentivirus into the rat intervertebral disc degeneration model. Results: Bioinformatics analysis indicated that MGST1 is a key candidate gene in IDD. MGST1 expression was consistently upregulated with increasing degeneration severity in rat disc tissues and degenerated NP cells. Knockdown of MGST1 significantly promoted extracellular matrix degradation and increased apoptosis and senescence levels in NP cells, while MGST1 overexpression markedly improved these changes. Mechanistic studies revealed that MGST1 deficiency significantly enhanced ferroptosis characteristics in NP cells, including accumulation of lipid peroxides and ROS, increased Fe2+ content, and decreased mitochondrial membrane potential. In vivo experiments demonstrated that MGST1 overexpression significantly alleviated the degree of IDD in rats. Conclusion: MGST1 exhibits compensatory upregulation during the progression of intervertebral disc degeneration and delays its progression by inhibiting ferroptosis in nucleus pulposus cells. This study reveals a novel mechanism by which MGST1 regulates ferroptosis in IDD and provides a potential molecular target for the prevention and treatment of IDD.
✓ 已验证
DOI
PubMed
高影响因子
ACS Applied Nano Materials
·
2026
·
IF 5.8
Liu Kai,Shen Hongliang,Li Jietao,Feng Yu,Zhou Chang,Jiang Anlong
Osteosarcoma remains a highly aggressive primary bone
malignancy,
and its clinical treatment is frequently limited by chemoresistance,
systemic toxicity, and insufficient tumor-specific drug accumulation.
To address these challenges, we developed an OS-7.9 aptamer-functionalized
ZIF-8 nanoscale platform for the targeted codelivery of sorafenib
(SFN) and GPX4 siRNA, designated O-SR-ZIF-8, with the intended application
of ferroptosis-based osteosarcoma therapy. The resulting nanoparticles
exhibited a uniform nanoscale size distribution, favorable colloidal
stability, high payload-loading capacity, and pH-responsive release
behavior. The ZIF-8 nanostructure remained relatively stable under
physiological conditions but promoted accelerated release of SFN and
GPX4 siRNA in acidic tumor-mimicking microenvironments, supporting
its suitability for tumor-localized delivery. Compared with nontargeted
formulations, O-SR-ZIF-8 markedly enhanced cellular internalization
in MG-63 osteosarcoma cells, inhibited cell proliferation, promoted
cell death, increased intracellular oxidative stress, and suppressed
migration and invasion. In a murine osteosarcoma xenograft model,
systemic administration of O-SR-ZIF-8 significantly restrained tumor
growth through GPX4 silencing and modulation of ferroptosis-related
signaling. Moreover, the nanoscale formulation exhibited favorable
biocompatibility, as evidenced by negligible hemolytic activity and
no obvious histopathological injury in major organs. Together, these
findings indicate that O-SR-ZIF-8 is an aptamer-guided nanoscale therapeutic
platform with potential in the treatment of osteosarcoma through targeted
delivery of sorafenib and GPX4 siRNA to silence genes and increase
oxidative stress associated with ferroptosis.
✓ 已验证
产品关联
DOI
高影响因子
ACS Biomaterials Science & Engineering
·
2025
·
IF 5.5
Juan Huang,Mingjing Yang,Xingyu Zhou,Jigang Luo,Xiaoxia Yan,Guanghui Lin,Shijie Li,Shihui Liu,Zhuoyue Song,Chunzhi Tang,Nenggui Xu,Tao Liu,Jian Liang
Drug repurposing has received increasing attention in the field of oncology drug development as an alternative strategy to de novo drug synthesis. Disulfiram (DSF) has a long history of clinical application in alcohol withdrawal, and recent studies have revealed that its metabolite diethyldithiocarbamate (DDTC) can be coordinated with copper ions in vivo to form Cu-DDTC complexes with anticancer activity. However, the insufficient in vivo stability of DSF remains a challenge. In this study, the nanomedicine Cu-BTC@DDTC with DDTC-Cu(I) chemical valence and polycrystalline structure was prepared by incorporation of DDTC into the nanosized metal–organic framework (MOF) Cu-BTC. The in vitro cellular evaluation results showed that Cu-BTC@DDTC exhibited high inhibition of tumor cell growth, migration, and invasion. Animal experiments on the xenograft tumor model further demonstrated the excellent antitumor activity and biosafety of Cu-BTC@DDTC, and the antitumor activity was found to be closely related to the regulation of the SLC7A11/GPX4 signaling pathway to induce ferroptosis. This study provides a feasible option for antitumor drug development based on a drug repurposing strategy.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·1-17
·
IF 3.9
Chen Dongzhui,Yin Feifei,Yang Pin,Xia Wanrong,Huang Yi,Feng Yue,Yang Li,Lin Shuqiang,Zhang Qiuyue
Bronchopulmonary dysplasia (BPD) is one of the most common respiratory diseases in preterm infants. Studies have shown that ferroptosis is involved in the pathogenesis of BPD, and thioredoxin-interacting protein (TXNIP)-mediated oxidative stress also plays a role in its development. The solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) signaling pathway is one of the key pathways regulating ferroptosis. This study aimed to investigate the mechanism by which TXNIP regulates SLC7A11/GPX4 pathway-mediated ferroptosis in BPD. Mice were randomly divided into ten treatment groups: Air, Hyperoxia, Hyperoxia + RSL3, Hyperoxia + Ferrostatin-1, Hyperoxia + Ad-shNC, Hyperoxia + Ad-shTXNIP, Hyperoxia + Ad-vector, Hyperoxia + Ad-TXNIP, Hyperoxia + Ad-shSLC7A11, and Hyperoxia + Ad-shTXNIP + Ad-shSLC7A11. Lung tissues were collected for hematoxylin and eosin (H&E) staining to observe pathological changes, and transmission electron microscopy (TEM) was used to examine mitochondrial morphology. Real-time quantitative polymerase chain reaction (qPCR) was performed to measure the mRNA expression of TXNIP, SLC7A11, and GPX4. Western blotting was used to analyze the protein levels of TXNIP, SLC7A11, and GPX4. GPX4 activity was determined using an enzyme-linked immunosorbent assay (ELISA). Additionally, glutathione (GSH), malondialdehyde (MDA), and ferrous iron (Fe 2+ ) levels in lung tissues were measured using corresponding detection kits. H&E staining and TEM confirmed successful modeling of lung injury after hyperoxia. MDA and Fe 2+ increased, GSH decreased, and GPX4 activity declined after hyperoxia. TXNIP mRNA and protein were upregulated by hyperoxia, while SLC7A11 and GPX4 were downregulated. Ferroptosis activation exacerbated lung injury, whereas inhibition alleviated it. TXNIP overexpression using adenovirus serotype 5 (Ad5) aggravated ferroptosis in BPD, and this was ameliorated by TXNIP knockdown. Knockdown of the upstream signal SLC7A11 increased ferroptosis in BPD, and simultaneous knockdown of TXNIP and SLC7A11 reversed the ferroptosis reduction. In conclusion, in the BPD model, TXNIP expression was increased, and TXNIP promoted ferroptosis by downregulating the SLC7A11/GPX4 pathway. These findings suggest that gene therapy targeting TXNIP knockdown using adenovirus as a vector may serve as a therapeutic strategy for BPD.
✓ 已验证
DOI
PubMed
高影响因子
FREE RADICAL RESEARCH
·
2025
·
IF 2.9
Doudou Lu,Ling Yuan,Zhaozhao Wang,Duojie Xu,Fandi Meng,Shumin Jia,Yahong Li,Weiqiang Li,Yi Nan
The prognosis of gastric cancer (GC) remains poor due to metastases and resistance to chemotherapy. Ferroptosis is a novel cell death regulation mode characterized by iron dependence and lipid peroxidation. Dioscin, a compound extracted from the Paris polyphylla rhizomes roots, has been shown to have an inhibitory effect on cancers. However, whether it induces ferroptosis to participate in anti-cancer metastasis remains unclear. The ability of gastric cancer cells to invade and migrate was evaluated by wound healing and transwell assays. Malondialdehyde (MDA), glutathione (GSH) assay kit, and dichlorofluorescin diacetate (DCFH-DA) fluorescent probes were used to detect ferroptosis in gastric cancer cells. The expression levels of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot methods. The rescue assay was performed by adding Ferrostatin-1 (Fer-1) co-treatment to verify that Dioscin inhibited gastric cancer metastasis by participating in ferroptosis. Dioscin inhibited gastric cancer cells’ wound healing, migration, and invasion process. In addition, Dioscin increased the level of reactive oxygen species (ROS) and MDA while decreasing GSH level, and induced ferroptosis of gastric cancer cells. Fer-1, an inhibitor of ferroptosis, could reverse the effect of Dioscin. In terms of mechanism, Dioscin induced ferroptosis through SLC7A11/GPX4 axis and was involved in the regulation of inhibiting metastasis of gastric cancer. These results suggested that Dioscin was involved in anti-cancer metastasis by inducing ferroptosis.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advances in Pharmacological and Pharmaceutical Sciences
·
2026
·Vol. 2026
·期 1
·7893262
·
IF 2.9
Jiaxiang Liao,Zitian Wang,Zhou Huang,Jincheng Li,Jie Yang,Chunyun Fang,Dongling Huang,Fan Wang,Xueling Lu,Yiling Zhai,Wei Wang
Myocardial infarction (MI) involves a pathological process in which its association with ferroptosis is notably pronounced, and targeted regulation of ferroptosis presents a promising approach for treating MI. This work delineates the molecular basis by which the natural sesquiterpene germacrone protects against cardiomyocyte ferroptosis following isoproterenol (ISO)-induced MI. We established a murine model of ISO-induced MI, paired with an injured H9c2 cardiomyocyte model in vitro. Mice in the experimental group received daily oral germacrone (25, 50, and 100 mg/kg) for 7 consecutive days. We profiled myocardial injury markers and key nuclear factor erythroid 2–related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) axis proteins. The mechanism of action was confirmed by utilizing ML385, the Nrf2-specific inhibitor. Germacrone significantly reduced ISO-induced myocardial injury in mice, improving cardiac function and decreasing myocardial histopathological damage. Germacrone universally attenuated the elevation of myocardial injury and inflammatory markers in all experimental models. It also decreased the apoptosis rate of H9c2 cells. Germacrone inhibited myocardial ferroptosis and upregulated the abundance of pivotal regulatory proteins, including Nrf2, GPX4, and heme oxygenase-1 (HO-1), along with solute carrier family 7 member 11 (SLC7A11). ML385, an Nrf2 antagonist, can block germacrone’s protective effect against ISO-induced myocardial ferroptosis and reverse its upregulation of these pathway proteins. These findings provide a new potential target and experimental foundation for MI treatment.
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2023
·
IF 6.1
Ming-Shan Chen,Jia-Xin Wang,Hao Zhang,Jia-Gen Cui,Yi Zhao,Jin-Long Li
Phthalates are widely used to improve the flexibility of poly(vinyl chloride) (PVC) polymer agriculture products. Di(2-ethylhexyl) phthalate (DEHP) is a type of addition to plastic and can lead to many health problems. Hemeoxygenase-1 (HO-1) is an extremely important molecule that releases enzymatic products to promote ferroptosis. This research aimed to explore the function of HO-1 in DEHP-induced renal proximal tubule cell ferroptosis. In the experiment, ICR male mice are exposed to (0, 50, 200, and 500 mg/kg BW/day) DEHP for 28 days. Here, we observed that DEHP induced glomeruli atrophy and the tubules swell. Furthermore, DEHP exposure could increase ferrous iron content and decrease antioxidant activity. We also found that DEHP exposure increased the expression of nuclear factor-erythroid 2 p45-related factor 2 (NFE2L2) in the nucleus. In particular, the expression of (HO-1) is significantly increased both in protein and mRNA levels. Glutathione peroxidase 4 (GPX4) as an endogenous control of ferroptosis was downregulated, which proved the occurrence of ferroptosis. In the study, exposure to DEHP activated the NFE2L2/HO-1 signaling pathway and resulted in ferroptosis of the proximal tubule. This research connects ferroptosis with HO-1, providing new insights into the potential roles of phthalates in nephrotoxicity.
研究领域:
毒理学
·
肾脏生理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
LIFE SCIENCES
·
2026
·
IF 5.1
Pan Huang,Kexin Zhang,Ying Chen,Jiaxin Cheng,Shuangshuang Yang,Lin Shi,Yajuan Wang,Qin Zhang
Elevated homocysteine (Hcy) is an independent risk factor for hypertension, and kidney is an important organ for Hcy metabolism and blood pressure regulation, and its damage is closely related to the process of hypertension. Recent evidence suggests that ferroptosis, an oxidative stress-related form of cell death, contributes significantly to hypertensive organ damage. However, whether Hcy aggravates renal injury in H-type hypertension by destroying renal hydrogen sulfide (H 2 S) metabolism and driving ferroptosis is still lack of direct evidence. In this study, the H-type hypertensive rat model induced by high methionine diet combined with HK-2 cell model was studied. We observed a significant increase in blood pressure and plasma Hcy in the Hcy group, accompanied by renal dysfunction and renal tubular injury. Specifically, in the renal tissue of Hcy group rats, the levels of KIM-1, Fe 2+ and malondialdehyde (MDA) were increased, glutathione/glutathione disulfide (GSH/GSSG) ratio decreased, SLC7A11 expression was down-regulated, and GPX4 activity was inhibited. Concurrently, H 2 S levels and cystathionine-beta-synthase (CBS) activity were decreased. In vitro experiments using HK-2 cells confirmed that Hcy could down-regulate the expression of CBS, cystathionine-gamma-lyase (CSE), SLC7A11, GPX4 and GSH/GSSG ratio, and up-regulate MDA and reactive oxygen species (ROS) levels. Treatment with H 2 S donor (NaHS) or ferroptosis inhibitors (Ferrostatin-1, Fer-1) could rescue these changes. Collectively, our results demonstrate that high Hcy promotes hypertension by suppressing endogenous H 2 S generation, downregulating the SLC7A11/GPX4 signaling axis, and inducing ferroptosis. These findings reveal a new mechanism by which Hcy aggravates hypertension by inhibiting H 2 S synthesis and inducing ferroptosis.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
LIFE SCIENCES
·
2026
·
IF 5.1
Wei Hua,Yilei Sun,Mingze Sun,Yiying Liu,Hongxue Sun,Huinan Chen,Shuainan Ma
Aims Neuronal ferroptosis affects the pathogenesis of diabetes-associated cognitive decline (DACD). Exogenous hydrogen sulphide (H 2 S) treatment ameliorates cognitive deficits in diabetic mice. This study aimed to explore whether H 2 S exerts neuroprotective effects by suppressing ferroptosis through activation of Nrf2/GPX4 signalling pathway. Materials and methods STZ-induced diabetic mice received NaHS or NaHS combined with the Nrf2 inhibitor ML385, after which cognitive functions were evaluated using the Morris water maze test. Hippocampal neuronal damage and mitochondrial morphological changes were identified using transmission electron microscopy, haematoxylin and eosin (H&E) staining, Nissl staining, and immunofluorescence staining. The expression levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and iron were determined using assay kits. Western blotting was performed to evaluate the expression of the Nrf2/GPX4 axis, iron transport-related proteins, and GSH synthesis enzymes. Key findings Exogenous H 2 S treatment ameliorated cognitive deficits by mitigating hippocampal neuronal loss and improving synaptic ultrastructural integrity. The levels of ROS, MDA, and iron were reduced, whereas SOD, GSH, and Nrf2/GPX4 expression were increased following NaHS administration. Exogenous H 2 S also ameliorated mitochondrial impairment and suppressed ferroptosis in the hippocampal neurones. However, these neuroprotective effects were abolished by ML385. Diabetic mice cotreated with ML385 and NaHS exhibited prolonged escape latency and reduced time in the target quadrant. Additionally, ML385 co-administration with NaHS exacerbated neuronal damage, oxidative stress, synaptic ultrastructural abnormalities, and iron dysregulation, while downregulating Nrf2/GPX4 expression and inhibiting ferroptosis suppression. Significance Exogenous H 2 S treatment alleviates DACD by suppressing ferroptosis via activation of the Nrf2/GPX4 signalling pathway.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）