INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Jie Chen,Dexian Li,Xiaohu Chen,Qiuxing He,Anna Zuo,Baizhao Peng,Ying Yang,Chuanghai Wu,Qinghong Chen,Zihao Jiang,Ziwei Li,Wen Fang,Jingxin Lin,Hiu Yee Kwan,Xiaomin Sun,Lin Zhou,Xiaoshan Zhao
Limonin alleviates hyperuricemia-induced cognitive impairment and neuroinflammation in UOX −/− rat models. • Limonin exerts neuroprotective effects by inhibiting microglial activation and subsequent neuronal apoptosis. • Limonin modulates the HIF-1α/iNOS pathway to exert anti-inflammatory and neuroprotective effects. Background Hyperuricemia (HUA), a highly prevalent metabolic disorder, is increasingly linked to cognitive impairment. Limonin (LIM), a natural compound with anti-inflammatory and neuroprotective properties, has the therapeutic benefits, but its underlying mechanisms remain unclear. Purpose This study aimed to investigate the therapeutic effect and mechanism of LIM on HUA-induced cognitive impairment. Methods A rat model of HUA-induced cognitive impairment was established using urate oxidase gene knockout (UOX −/− ) rat. Uric acid (UA) levels of serum and cerebrospinal fluid (CSF) were measured to confirm hyperuricemia. Cognitive function was assessed using morris water maze test, while neuronal morphology and synaptic integrity were evaluated via Nissl staining and synaptic plasticity biomarkers. Microglial activation and polarization were examined through double immunofluorescence staining of CD86/IBA1 and ARG1/IBA1, inflammatory and oxidative stress markers were quantified using ELISA, qRT-PCR and Western blot. In vitro , BV2 microglial cells were stimulated with UA to model activation and inflammatory responses. HT22 neuronal cells were co-cultured using conditioned medium to assess apoptosis via TUNEL assay and expression of apoptosis-related biomarkers. RNA sequencing was performed to identify key signaling pathways modulated by LIM, and the findings were validated through targeted gene overexpression or inhibition experiments. Results The UOX −/− rat model successfully recapitulated HUA-induced cognitive impairment, as evidenced by elevated UA levels, alongside significant cognitive deficits. LIM treatment ameliorated these cognitive impairments, attenuated neuropathological alterations, modulated microglial M1/M2 polarization, and reduced neuroinflammation and oxidative damage. In vitro , LIM suppressed UA-induced microglial activation and inflammatory response, while also rescuing neuronal apoptosis in HT22 cells. RNA sequencing revealed involvement of the HIF-1 pathway. HIF-1α inhibitor YC-1 enhanced LIM's effects, whereas HIF-1α activator DMOG reversed them, suggesting that the modulation of the HIF-1α/iNOS pathway contributes to redox homeostasis and neuroinflammation. Conclusion LIM ameliorates HUA-induced cognitive impairment by suppressing microglial activation and neuroinflammation, which is associated with the inhibition of the HIF-1α/iNOS signaling pathway, underscoring its therapeutic potential. Download: Download high-res image (110KB) Download: Download full-size image
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高影响因子
Chinese Medicine
·
2026
·Vol. 21
·期 1
·154
·
IF 7.4
Ding Wei,Zhang Ni,Xiao Lei,Yu Le,Wu Tian-Shi,Feng Yuan-Jie,Chen Wei
Background Hypertrophic cardiomyopathy (HCM) is often complicated by coronary microvascular dysfunction (CMD), which precipitates localized myocardial ischemia and metabolic disturbance, triggering compensatory cardiomyocyte hypertrophy. This hypertrophy, in turn, exacerbates microvascular insufficiency, forming a pathological feedback loop and culminating in persistent cellular stress, inflammatory infiltration, and myocardial fibrosis. This “ischemia–hypertrophy–inflammation–fibrosis” interrelationship not only drives pathological remodeling but also significantly elevates the risk of heart failure, arrhythmias, and adverse prognosis. The traditional formula Huayu Qutan Formula (HYQT), used clinically for years, has been shown to significantly enhance cardiac function in HCM patients. However, its underlying mechanisms remain poorly elucidated. This study aims to explore HYQT’s therapeutic effects on HCM and to reveal its intrinsic mechanisms. Methods Blood-absorbed constituents of HYQT were identified using UHPLC-MS, followed by network pharmacology analysis and molecular docking to predict potential targets and key signaling pathways. An isoproterenol (ISO)-induced HCM mouse model, along with parallel in vitro injury models using H9C2 cardiomyocytes and human cardiac microvascular endothelial cells (HCMECs), was established to systematically assess the in vivo and in vitro effects of HYQT. To comprehensively evaluate HYQT’s modulation of myocardial hypertrophy, fibrosis, and angiogenesis, echocardiography, laser speckle perfusion imaging, immunohistochemistry, western blotting, reactive oxygen species (ROS) assays, and wound-healing assays were performed. Results UHPLC-MS analysis identified 31 blood-absorbed bioactive components of HYQT. Integrated network pharmacology and molecular docking analyses identified the MAPK and HIF-1α-signaling pathways as key therapeutic targets. In ISO-induced HCM mice, HYQT significantly improved cardiac morphology and function, reduced hypertrophic markers (ANP and BNP), inhibited myocardial collagen deposition, attenuated fibrosis, restored microvascular perfusion and density, and suppressed oxidative stress (MDA and ROS) and pro-inflammatory cytokine expression (TNF-α and IL-6). Mechanistically, in vitro experiments supported a cell-type–resolved, parallel regulatory effect: in HCMECs, HYQT-containing serum enhanced migration and viability, reduced ROS accumulation, and activated HIF-1α/VEGF-mediated angiogenic signaling, thereby alleviating microvascular dysfunction; concurrently, in H9C2 cardiomyocytes, HYQT inhibited phosphorylation of ERK, p38, and JNK, restored mitochondrial membrane potential, and reduced cell death, thereby mitigating hypertrophic remodeling and its downstream fibrotic progression. Conclusion HYQT effectively ameliorates key pathological features of HCM, including myocardial hypertrophy, fibrosis, and microvascular dysfunction. As a clinically used herbal formulation, this study provides mechanistic insight into its therapeutic effects by revealing a cell-type–resolved, myocardium–microvasculature regulatory framework. Specifically, HYQT suppresses MAPK signaling to attenuate cardiomyocyte hypertrophy while enhancing HIF-1α–mediated angiogenesis to improve the microvascular environment. These simultaneous effects are associated with mitigation of pathological cardiac remodeling, suggesting that HYQT may serve as a promising multi-target therapeutic strategy for HCM.
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高影响因子
FASEB JOURNAL
·
2026
·Vol. 40
·期 14
·e72154
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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.
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CELLULAR SIGNALLING
·
2025
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IF 3.7
Jiaoquan Chen,Hui Zou,Bihua Liang,Yeqing Gong,Shaoyin Ma,Runxiang Li,Jiacong Zeng,Chao Bi,Huilan Zhu
Drug resistance poses a significant challenge in the clinical management of melanoma, primarily driven by the hypoxic tumor microenvironment. This study aims to elucidate the molecular mechanisms underlying drug resistance in melanoma under hypoxic conditions. Exosomes were isolated from melanoma cells cultured under normoxic (Nor-exos) and hypoxic (Hypo-exos) environments. The proliferative capacity of tumor cells was assessed using CCK-8 and colony formation assays, while relevant molecular expressions were evaluated through qPCR, Western blotting, immunofluorescence, and immunohistochemistry. Additionally, mitochondrial damage was examined via transmission electron microscopy, and reactive oxygen species (ROS) levels were quantified using flow cytometry. Xenograft models further facilitated the investigation into the molecular mechanisms of drug resistance. Hypo-exos promote drug resistance in melanoma cells by inhibiting ferroptosis; mechanistically, Hypo-exos inhibiting p53 and OTUB1 expression through HIF-1α transfer. Furthermore, OTUB1 enhances SLC7A11 stability, thereby reducing ferroptosis levels and fostering drug resistance in melanoma. Our findings indicate that Hypo-exos inhibit ferroptosis to augment drug resistance in melanoma by delivering HIF-1α to modulate the p53/OTUB1/SLC7A11 axis. Exosomal HIF-1α may represent a promising biomarker and therapeutic target for addressing drug resistance in melanoma.
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ENVIRONMENTAL POLLUTION
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2022
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IF 9.988
Jiawei Huang,Yunqiu Pu,Kai Xu,Qin Ding,Rongli Sun,Lihong Yin,Juan Zhang,Yuepu Pu
Benzene exposure can cause pancytopenia and immunosuppression , leading to serious diseases such as aplastic anemia (AA) or acute myeloid leukemia (AML), but the underlying mechanism has not been fully elucidated. Hypoxia-inducible factor 1 (HIF-1) is an important transcription factor that regulates many downstream target genes. In this study, we reported a novel mechanism by which high expression of HIF-1α alleviated benzene toxicity. Mice with high expression of HIF-1α (HIF-1α + ) were obtained by the Tet-on system and doxycycline induction, and they and wild-type (WT) mice were exposed to 150 mg/kg benzene for 0, 1, 3, 7, 10, 14, and 28 days. Dynamic changes in hematopoietic and immune-related indicators and the role of HIF-1α were explored. The level of white blood cells in mice reached the highest level on the third day, and immunity was activated and then suppressed within 10 days. Significant pancytopenia and immunosuppression occurred at 14 days and were more pronounced at 28 days. The levels of HIF-1α, EPO, VEGF, RORγt, and IL-17 in WT mice gradually decreased with increasing benzene exposure days, while the levels of Foxp3 and IL-10 increased. These changes were alleviated in HIF-1α + mice. High expression of HIF-1α increased the levels of EPO and VEGF, which helped to maintain the stability of the hematopoietic microenvironment. Simultaneously, it attenuated benzene-induced immunosuppression by alleviating the Th17/Treg imbalance. HIF-1α is expected to be a new target for benzene-induced diseases such as AA and AML.
研究领域:
毒理学
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免疫学
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血液学
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分子生物学
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
Yongshuai Jing,Mingsong Li,Yingqi Li,Teng Ma,Ying Qu,Beibei Hu,Yinghua Xie,Zhiwei Li
This study aimed to characterize the structure of polysaccharide ZOPA extracted from Zingiber officinale and its purified form (ZOPA-1), and to investigate their anti-fatigue mechanisms based on the gut-muscle axis. The study found that the backbone of ZOPA-1 is primarily composed of →3,4)-α-Glcp-1→ and →4,6)-α-Glcp-(1→ linkages, with →4)-α-Glcp(1→ serving as its side chain. In exhaustive swimming experiments with mice, both crude ZOPA and purified ZOPA-1 demonstrated significant anti-fatigue effects, including enhanced glycogen storage, improved antioxidant capacity, reduced accumulation of metabolic waste products, and regulated energy metabolism in the gastrocnemius muscles. These effects may be mediated through the activation of the Keap1-Nrf2/ARE and AMPK/PGC-1α signaling pathways. Furthermore, ZOPA and ZOPA-1 modulated the intestinal flora of mice, increasing diversity, altering abundance, and regulating short-chain fatty acid concentrations, suggesting a potential role of the gut-muscle axis in mediating the anti-fatigue effects. This study provides valuable insights into the complex interplay between polysaccharides, the gut-muscle axis, and exercise-induced fatigue.
研究领域:
食品科学
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运动医学
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营养学
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Bioactive Materials
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2025
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IF 20.3
Shengming Zhang,Weixian Hu,Yanzhi Zhao,Yuheng Liao,Kangkang Zha,Wenqian Zhang,Chenyan Yu,Jiewen Liao,Hui Li,Wu Zhou,Faqi Cao,Bobin Mi,Guohui Liu
Fracture healing in patients with type 2 diabetes mellitus (T2D) is markedly impaired, characterized by a prolonged inflammation phase and defective osteoblast differentiation at the fracture site. In this study, we identified aberrant cellular glycolysis at T2D fracture sites, with bone marrow mesenchymal stem cells (BMSCs) exhibiting suppressed glycolysis and macrophages displaying enhanced glycolysis, mediated by the dysregulation of hypoxia-inducible factor-1α (HIF-1α). To rectify these metabolic imbalances, we developed a multifunctional nanocomposite PN@MHV hydrogel. Myricitrin, a flavonoid glycoside, forms the MHV hydrogel by cross-linking with HA-PBA and PVA via hydrogen bonds, and upregulates glycolysis through HIF-1α, thus promoting osteoblast differentiation under high glucose environment. To further regulate the inflammatory microenvironment, we incorporated nanoparticles loaded with PX-478, a HIF-1α specific inhibitor, into the hydrogel, with folic acid covalently modified to target proinflammatory M1 macrophages. This PN@MHV hydrogel bidirectionally regulated glycolysis via HIF-1α, enhancing osteoblast differentiation while attenuating macrophage-mediated inflammation. Comprehensive in vitro and in vivo experiments in a T2D fracture mouse model confirmed the hydrogel's ability to improve the inflammatory microenvironment and accelerate bone healing. Our findings underscore the therapeutic potential of targeting cellular glycolysis as a promising approach for enhancing fracture healing in diabetic patients.
研究领域:
医学
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生物材料学
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代谢生物学
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高影响因子
Acta Pharmaceutica Sinica B
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2021
·
IF 11.614
Yang Zhou,Fan Tong,Weilong Gu,Siqin He,Xiaotong Yang,Jiamei Li,Yue-Dong Gao,Huile Gao
Considering that photodynamic therapy (PDT)-induced oxygen consumption and microvascular damage could exacerbate hypoxia to drive more glycolysis and angiogenesis, a novel approach to potentiate PDT and overcome the resistances of hypoxia is avidly needed. Herein, morpholine-modified PEGylated bilirubin was proposed to co-deliver chlorin e6, a photosensitizer, and diclofenac (Dc). In acidic milieu, the presence of morpholine could enable the nanocarriers to selectively accumulate in tumor cells, while PDT-generated reactive oxidative species (ROS) resulted in the collapse of bilirubin nanoparticles and rapid release of Dc. Combining with Dc showed a higher rate of apoptosis over PDT alone and simultaneously triggered a domino effect, including blocking the activity and expression of lactate dehydrogenase A (LDHA), interfering with lactate secretion, suppressing the activation of various angiogenic factors and thus obviating hypoxia-induced resistance-glycolysis and angiogenesis. In addition, inhibition of hypoxia-inducible factor-1 α (HIF-1 α ) by Dc alleviated hypoxia-induced resistance. This study offered a sequentially responsive platform to achieve sufficient tumor enrichment, on-demand drug release and superior anti-tumor outcomes in vitro and in vivo .
研究领域:
癌症治疗
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纳米技术
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药学
·
分子生物学
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ACS Nano
·
2021
·
IF 15.881
Ping Wang,Qingshuang Tang,Lulu Zhang,Menghong Xu,Lihong Sun,Suhui Sun,Jinxia Zhang,Shumin Wang,Xiaolong Liang
Hypoxia in a solid tumor microenvironment (TME) can lead to the overexpression of hypoxia-inducible factor-1α (HIF-1α), which correlates to tumor metastasis. Reactive oxygen species (ROS) induced tumor cell apoptosis is becoming a promising method in tumor treatment. Currently, the ROS generating systems, e.g., photodynamic treatment and sonodynamic treatment, highly depend on oxygen (O2) in the tumor microenvironment (TME). However, the level of O2 in TME is too low to produce enough ROS. Herein, we developed an ultrasmall DSPE-PEG2000 coated barium titanate nanoparticle (P-BTO) for tumor treatment based on ultrasound triggered piezocatalysis and water splitting. Interestingly, irradiated by ultrasound, the surface of ultasmall P-BTO nanoparticles produced imbalance charges, which induced a cascade of redox reaction processes to simultaneously generate ROS and O2, the latter one was hardly generated in large-sized barium titanate nanoparticles. The as-synthesized P-BTO reached the highest accumulation in the tumor site at 4 h after intravenous injection. The results showed that the produced O2 significantly alleviated the hypoxia of TME to down-regulate the expression of HIF-1α, and the produced ROS can efficiently kill tumor cells. Moreover, the tumor metastasis was also inhibited, providing a different way to treat triple-negative breast cancer, which was easily metastatic and lacked effective treatments in the clinic.
研究领域:
纳米技术
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癌症治疗
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生物医学工程
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材料科学
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高影响因子
PHARMACOLOGICAL RESEARCH
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2022
·
IF 10.334
Chan Li,Yao-Hao Xu,Yu-Tao Hu,Xiu Zhou,Zhi-Shu Huang,Ji-Ming Ye,Yong Rao
Promoting energy expenditure is known to curb obesity and can be exploited for its treatment. Our previous study has demonstrated that activation of HSF1/PGC-1α axis efficiently induced mitochondrial biogenesis and adaptive oxidation and thus ameliorating lipid accumulation, however, whether it can be a therapeutic approach for metabolic disorders treatment needs explored. Here, a high-efficient and specific HSF1/PGC-1α activator screening system was established and the natural clinical liver-protecting agent matrine was identified as a robust HSF1/PGC-1α activator. Matrine treatment efficiently induced mitogenesis and thermogenic program in primary mouse adipose stem cell derived adipocytes by enriching HSF1 to the promoter of Pgc-1α . Deficiency of PGC-1α in adipocytes diminished the browning induction ability of matrine. Oral administration of matrine to the obese mice induced by high fat and high cholesterol diet increased energy expenditure and corrected the degeneration of thermogenesis in brown adipose tissue (BAT). Also, matrine treatment markedly induced the transformation of brown-like adipocytes in subcutaneous white adipose tissue (sWAT) via a mechanism of HSF1/PGC-1α, thereby attenuating obesity and myriads of metabolic disorders. This led to an improvement in adaptive thermogenesis to cold stimuli. These findings are of great significance in understanding the regulation mechanisms of the HSF1/PGC-1α axis in thermogenesis and providing a novel therapeutic approach for obesity treatment. Matrine may have potential therapeutic implications for the treatment of obesity in clinics.
研究领域:
药理学
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代谢学
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分子生物学
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高影响因子
CLINICAL SCIENCE
·
2022
·Vol. 136
·期 22
·1711-1730
·
IF 6.876
Gao Shuya,Yang Qingchen,Liu Zekun,Kong Weixian,Chen Jiawen,Li Xie,Peng Yue,Bao Mengmeng,Bian Xiaohong,Zhang Yuexin,Jiang Qizhou,Li Zhe,Zhang Yubin,Yan Fangrong,Ye Junmei
Metformin is accepted as a first-line drug for the therapy of Type 2 diabetes (T2D), while its mechanism is still controversial. In the present study, by taking advantage of mouse model of high-fat-diet (HFD)-induced obesity and primary mouse hepatocytes (PMHCs) as well as human hepatocyte L02 cell line, we aimed to investigate the involvement of SIRTs during the application of metformin for the therapy of T2D. Our data evidenced that during HFD-induced obesity, there was elevation of nucleus protein acetylation. Analysis of liver tissue showed that among all SIRT members, SIRT6 expression was significantly down-regulated during HFD feeding, which was sustained to regular level with metformin administration. Our result also showed that SIRT6 suppressed intracellular oxidative stress upon FAs stimulation in PMHCs and L02 cells. Mechanistically, SIRT6, but not SIRT1 promoted PGC-1α expression. We further prove that ENDOG is downstream of PGC-1α. In addition, we evidenced that ENDOG protects hepatocytes from lipid-induced oxidative stress, and down-regulation of Endog blunted the protective role of metformin in defending against FAs-induced oxidative stress. Our study established a novel mechanism of metformin in counteracting lipid-induced hepatic injury via activating SIRT6/PGC-1α/ENDOG signaling, thus providing novel targets of metformin in the therapy of T2D.
研究领域:
药理学
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内分泌学
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分子生物学
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细胞生物学
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高影响因子
Journal of Gastrointestinal Oncology
·
2025
·Vol. 16
·期 6
·2703
·
IF 2
Tang Pingfei,Wu Yueming,Tan Lin,Zhang Chao,Qin Liping,Wu Dajun
Background Our preliminary experiments confirmed that follistatin-like 3 (FSTL3) expression is elevated in colorectal cancer (CRC) cells following CoCl 2 treatment. In this study, we investigated the regulatory role of FSTL3 in CRC progression and the molecular mechanisms underlying its high expression. Methods CoCl 2 (150 µM) was used to mimic hypoxia. Cell proliferation was measured by colony formation assay, wound healing assays were performed to assess cell migration, and Transwell assays were performed to evaluate invasion. The glucose metabolism pathways were assessed by detecting extracellular acidification rate, oxygen consumption rate, glucose uptake, and lactate production. The binding sites of zinc finger protein 454 (ZNF454) and FSTL3 gene promoter were analyzed by JASPAR databases, and were confirmed by chromatin immunoprecipitation (ChIP) and luciferase reporter assay. The expression levels of molecules at mRNA and protein levels were determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. Results We found that both FSTL3 and hypoxia-inducible factor 1α (HIF-1α) were upregulated in CRC tissues and in CRC cells under hypoxic conditions, with a positive correlation between their expression in clinical samples. Silencing FSTL3 reduced HIF-1α expression and suppressed the expression of glycolytic enzymes (glucose transporter 1, hexokinase 2, lactate dehydrogenase A, and pyruvate kinase muscle isozyme M2). Knockdown of FSTL3 increased oxygen consumption while decreasing extracellular acidification, glucose uptake, and lactate production. Moreover, FSTL3 downregulation markedly inhibited the proliferation, migration, and invasion of CoCl 2 -treated CRC cells. We further identified ZNF454 as a potential transcription factor for FSTL3 and confirmed its binding to the FSTL3 promoter. Upregulation of ZNF454 significantly suppressed CRC cell proliferation, migration, invasion, and glycolysis, effects that were reversed by FSTL3 overexpression. In vivo , ZNF454 overexpression effectively inhibited tumor growth and reduced HIF-1α and glycolytic enzyme expression, whereas these effects were rescued by FSTL3 overexpression. Conclusions Collectively, our findings demonstrate that ZNF454 suppresses CRC development by inhibiting FSTL3/HIF-1α-mediated glycolysis through transcriptional repression of FSTL3. This study is the first to reveal the molecular mechanism responsible for FSTL3 overexpression in CRC, providing a novel perspective for CRC treatment.
研究领域:
肿瘤学
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分子生物学
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癌症代谢
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转录调控
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细胞信号传导
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危险品化学品经营许可证（带存储）