INTERNATIONAL IMMUNOPHARMACOLOGY
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2025
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IF 4.7
Wenyao Yang,Juanzhu Han,Liping Zhang,Yunsong Sun,Yuchen Zhu,Yiyu Liu,Jingyu Chen,Xiaoyao Liao,Hui Liao,Weizhuo Xu,Yongbo Song
Skeletal muscle inflammation associated with sepsis has been identified as a critical pathological process contributing to metabolic dysfunction and poor clinical outcomes. Voltage-gated sodium channels (VGSCs) have been implicated in immune modulation; however, their specific roles in skeletal muscle inflammation remain poorly understood. In this study, the VGSC subtype Nav1.5 was investigated as a potential regulator of inflammation, and the therapeutic efficacy of a novel recombinant scorpion peptide, DKK678, was evaluated. An in vitro model using lipopolysaccharide (LPS)-stimulated C2C12 cells and an in vivo cecal ligation and puncture (CLP) model in septic mice were established. In both models, Nav1.5 expression was significantly upregulated in response to inflammatory stimuli, while Nav1.4 expression remained unchanged. The nuclear factor kappa B (NF-κB) signaling pathway was found to be activated, contributing to increased expression of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), adhesion molecules (VCAM-1), and gap junction proteins (Cx43). Suppression of VGSC activity using lidocaine resulted in the inhibition of NF-κB phosphorylation and downregulation of inflammatory markers, while the expression of interleukin-10 (IL-10) and interleukin-4 (IL-4) were restored. Tetrodotoxin (TTX) treatment did not replicate these effects, suggesting Nav1.5-specific involvement. DKK678 was developed through bioinformatic design and molecular docking simulations, which predicted a stronger binding affinity and structural stability with Nav1.5 compared to Nav1.4. These predictions were validated through functional experiments. In vitro, DKK678 treatment dose-dependently inhibited LPS-induced NF-κB pathway activation and reversed abnormal expression of VCAM-1 and Cx43. In vivo, DKK678 significantly ameliorated CLP-induced skeletal muscle damage, suppressed inflammatory cytokine production, and improved tissue histopathology. Furthermore, the structural integrity of immune organs such as the thymus and spleen was preserved in DKK678-treated septic mice, with partial restoration of lymphocyte populations and organ indices. Notably, Nav1.5 expression was downregulated by DKK678, while Nav1.4 expression remained unaffected. These results demonstrate that Nav1.5 serves as a critical inflammatory modulator in skeletal muscle and immune tissues. Its upregulation was shown to drive NF-κB pathway activation and inflammatory cytokine production. By targeting Nav1.5, DKK678 was able to exert dual protective effects on both skeletal muscle and immune organs under septic conditions. The therapeutic potential of DKK678 was found to be comparable to that of dexamethasone (DEX) at high doses, without altering Nav1.4 expression. In conclusion, the present study provides new mechanistic insight into the role of Nav1.5 in skeletal muscle inflammation and identifies DKK678 as a promising peptide therapeutic that targets Nav1.5 to suppress NF-κB-mediated inflammatory injury. These findings suggest that Nav1.5 inhibition represents a viable strategy for the treatment of sepsis-associated myositis and related inflammatory disorders.
研究领域:
免疫学
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药理学
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分子生物学
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病理学
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DOI
PubMed
高影响因子
CLINICAL IMMUNOLOGY
·
2025
·
IF 3.8
Shuang Pan,Mengshu Yu,Bowei Fan,Bin Wang,Xinrui Yang,Jiawen Zhang,Xiaoqi Liu,Xiaojian Hong,Wei Yang
Autoimmune myocarditis refers to the inflammation of myocardial tissue caused by innate and adaptive immune responses, characterized by elevated levels of tumour necrosis factor-α (TNF-α), a classic pro-inflammatory factor. Although hydrogen exhibits anti-inflammatory and antioxidant properties, its therapeutic effects in autoimmune myocarditis have not been evaluated. Therefore, the present study aimed to explore whether hydrogen can alleviate autoimmune myocarditis via TNF-α. An experimental autoimmune myocarditis (EAM) model was established in BALB/c mice via subcutaneous injection of pig-derived myocardial myoglobin emulsified with complete Freund's adjuvant. The treatment group received 2 % hydrogen inhalation twice a day (3 h each time) for 21 days. CD4+ T cell expression was higher in the EAM group than in the Control group, and this increase was attenuated following treatment with hydrogen. Additionally, the levels of TNF-α and related inflammatory factors were substantially higher in the EAM group than in the Control group, and these changes were reversed following hydrogen treatment. Echocardiography assessments demonstrated a significant improvement in heart function following treatment with hydrogen compared to that in the EAM group. Pathological results revealed significant inflammatory cell infiltration and fibrosis in the hearts of the untreated EAM group. Tissue immunofluorescence and protein immunoblotting indicated elevated necroptosis markers in the EAM group, which were downregulated after treatment with hydrogen. This study demonstrates that hydrogen effectively ameliorated autoimmune myocarditis by modulating necroptosis via the TNF/TNFR1 signalling pathway, making it a promising novel therapeutic strategy for myocarditis.
研究领域:
免疫学
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心脏病学
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分子生物学
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炎症研究
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DOI
PubMed
高影响因子
INFLAMMATION
·
2019
·Vol. 42
·期 4
·1179-1189
·
IF 2.939
Xue Yu-Long,Zhang Sheng-Xiao,Zheng Chao-Feng,Li Yu-Feng,Zhang Li-Hui,Hao Yu-Fei,Wang Shu,Li Xue-Wen
Signal transducer and activator of transcription 4 (STAT4) has been implicated in the progression of myocarditis. The aim of the current study was to investigate the role by which STAT4 influences autoimmune myocarditis in an attempt to identify a theoretical therapeutic perspective for the condition. After successful establishment of an autoimmune myocarditis rat model, the expression patterns of STAT4, NF-κB pathway–related genes, Th1 inflammatory cytokines (IFN-γ and IL-2), and Th2 inflammatory cytokines (IL-6 and IL-10) were subsequently determined. The rats with autoimmune myocarditis were treated with oe-STAT4 or sh-STAT4 lentiviral vectors to evaluate the role of STAT4 in autoimmune myocarditis, or administrated with 1 mL 10 μmol/L of BAY11-7082 (the NF-κB pathway inhibitor) via tail vein to investigate the effect of the NF-κB pathway on autoimmune myocarditis. Finally, cell apoptosis was evaluated. The serum levels of IFN-γ and IL-2, extent of IκBα and P65 phosphorylation, and the expression of STAT4 were elevated, while the serum levels of IL-6 and IL-10 as well as the expression of IκBα were reduced among the rats with autoimmune myocarditis, which was accompanied by an increase in the apoptotic cells. More importantly, the silencing of STAT4 or the inhibition of the NF-κB pathway was detected to result in a decrease in the serum levels of IFN-γ and IL-2 and an elevation of the serum levels of IL-6 and IL-10, and inhibited myocardial cell apoptosis in rats with autoimmune myocarditis. Moreover, STAT4 silencing was also observed to decrease the extent of IκBα and P65 phosphorylation while acting to elevate the expression of IκBα. Taken together, silencing of STAT4 could hinder the progression of autoimmune myocarditis by balancing the expression of Th1/Th2 inflammatory cytokines via the NF-κB pathway, which may provide a novel target for experimental autoimmune myocarditis (EAM) treatment.
研究领域:
免疫学
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心脏病学
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分子生物学
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DOI
PubMed
高影响因子
TRANSPLANT IMMUNOLOGY
·
2025
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IF 1.4
Lei Zhang,Junjie Xu,Fujiang Cui,Jin Jin,Liwen Liu,Lei Wang,Yuxia Gao
Background Myocardial ischemia/reperfusion (I/R) injury is a common cause of death. FXYD domain-containing ion transport regulator-5 (Fxyd5) is a type I membrane protein that plays a significant role in mediating cellular functions. However, the expression and function of Fxyd5 in myocardial I/R injury remain unclear. Methods Male C57BL/6 mice (8–10 weeks) were subjected to myocardial I/R by ligating the left anterior descending coronary artery. Preventive intervention was performed using adeno-associated virus 9 (AAV9)-mediated Fxyd5 knockdown. An in vitro hypoxia/reoxygenation (H/R) in H9c2 cardiomyoblasts was used for validation. Results Myocardial I/R injury significantly upregulated Fxyd5 expression ( p < 0.01). Silencing Fxyd5 markedly improved cardiac function, as evidenced by a 58.0 % increase in EF ( p < 0.01) and a 54.5 % reduction in infarct size ( p < 0.01). Fxyd5 knockdown also attenuated myocardial apoptosis and inflammation, demonstrated by decreased cleaved caspase-3 expression and reduced levels of IL-6 (−44.2 %) and TNF-α (−42.7 %) ( p < 0.01). Mechanistically, Fxyd5 silencing suppressed NF-κB activation, and these protective effects were confirmed in vitro in H/R-treated cardiomyocytes. Conclusion Fxyd5 silencing significantly attenuated I/R-induced myocardial injury, reduced infarct size, and improved cardiac function, while also decreasing apoptosis and inflammatory cytokine expression ( p < 0.01). These findings indicate that Fxyd5 contributes to the pathogenesis of myocardial I/R injury and that its inhibition confers cardioprotective effects, partly through suppression of the NF-κB pathway.
研究领域:
心脏病学
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分子生物学
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炎症研究
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基因治疗
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细胞信号传导
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2017
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IF 2.956
Jia-Ying Zhang,Zheng Yang,Kun Fang,Zhan-Li Shi,Dan-Hong Ren,Jing Sun
Oleuropein (OLE) is a natural secoiridoid that is derived from Olea europaea . OLE possesses cardioprotective effects in experimental models of hypertension, myocardial infarction, atherosclerosis and hyperlipidaemia . In the present study, the effects of OLE on experimental autoimmune myocarditis (EAM) were evaluated. EAM in rats were induced by subcutaneous injections of porcine cardiac myosin . Cardiac function parameters, myocardial pathology, myocardial inflammatory cell infiltration and nuclear factor kappa-B (NF-κB) expression were measured. Our data showed that the postmyocarditis rats exhibited increased left ventricular end systolic diameters, left ventricular end diastolic diameters, left ventricular end-diastolic pressures (LVEDP), and decreased ejection fractions . However, OLE significantly suppressed these changes in EAM rats. Histological analysis revealed that myosin induced miliary foci of discolouration on endocardial surfaces and extensive myocardial injuries with inflammatory cell infiltration were significantly improved by OLE therapy. A definitive positive correlation between the histological scores and LVEDP was observed. Moreover, OLE inhibited CD4 + , CD8 + cells and macrophage infiltration in myocardium and decreased the serum production of tumour necrosis factor-a (TNF-a), interleukin-1β (IL-1β) and IL-6 in EAM rats. Expectedly, the myocardial levels of NF-κB p65, p-IκBa, IKKa were significantly attenuated by OLE, indicating the inhibitory effects of OLE on the NF-κB pathway. Furthermore, OLE decreased the myocardial expressions of phosphorylated-p38 MAPK , phosphorylated-ERK, and did not change the levels of p38 MAPK and ERK in EAM rats. Collectively, our results suggest that OLE effectively prevents the development of myocarditis , at least in part, by inhibiting the MAPKs and NF-κB mediated inflammatory responses.
研究领域:
药理学
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免疫学
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心脏病学
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DOI
PubMed
高影响因子
Nanoscale Research Letters
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2021
·Vol. 16
·期 1
·1-16
·
IF 4.703
Zhou Lin,Huang Zhi,Yang Shanyi,Wei Jiarui,Xu Yan,Hu Lin,Guo Xinrong,Yuan Limin,Yuan Zexuan,Yang Xiaoping,Tao Xiaojun,Zhang Qiufang
Hydrophilic polyethylene glycol monomethyl ether (mPEG) was grafted onto Icariin (ICA) by succinic anhydride to form a polyethylene glycol-Icariin (mPEG-ICA) polymer. The structure of the polymer was characterized by Fourier transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance spectroscopy (NMR). mPEG-ICA nanoparticles loaded with ICA were prepared by physical embedding of ICA by dialysis. The particle size was determined to be (220 ± 13.7) nm, and the ζ potential was (2.30 ± 1.33) mV by dynamic light scattering (DLS). Under a transmission electron microscope (TEM), the nanoparticles were spherical, and the morphology was regular. In the medium with pH 7.4, the drug release rate of mPEG-ICA nanoparticles reached (52.80 ± 1.70)% within 72 h. At pH 6.8, the cumulative drug release of nanoparticles reached (75.66 ± 0.17)% within 48 h. Treatment of the nanoparticles with LPS-treated H9c2 cells maintained cell viability, reduced LDH release and exerted antiapoptotic effects. Moreover, ICA-loaded mPEG-ICA nanoparticles significantly decreased the mRNA expression of the myocardial inflammatory cytokines TNF-α, IL-1β and IL-6M. In conclusion, ICA-loaded mPEG-ICA nanoparticles protected against LPS-induced H9c2 cell injury.
研究领域:
药学
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纳米技术
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细胞生物学
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炎症研究
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产品关联
DOI
PubMed
高影响因子
Frontiers in Genetics
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2022
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IF 4.772
Jiahui Chen,Jiadai Zheng,Nan Zheng,Rui Zhou,Lipin Huang,Jian He,Wenzong Zhu,Riyuan Zhang
Objective: The purpose of this study was to study the role and mechanism of miR-19b-3p in regulating myocardial inflammation and injury of viral myocarditis in viral myocarditis induced by Coxsackievirus B3 (CVB3). A CVB3 infection mouse model was established, the survival rate of mice was recorded after different treatments, cardiac function was detected, the degree of myocardial inflammatory infiltration and injury was detected by immunohistochemical and biochemical analyses, miR-19b-3p and PKNOX1 expression in cardiac tissue and cardiac infiltrating macrophages was detected using RT-PCR, and isolated mouse bone marrow-derived macrophages and the differentiation of macrophages after different transfections were detected. Finally, the binding of miR-19b-3p and PKNOX1 was verified by the dual luciferase reporter gene. The results showed that the expression of miR-19b-3p was significantly downregulated in the cardiac tissue and infiltrating macrophages of CVB3-infected mice, while the expression of PKNOX1 was upregulated. Upregulation of miR-19b-3p has protective effects against CVB3-induced myocardial injury in mice, such as weight gain, prolonged survival, increased left ventricular ejection fraction and left ventricular short axis shortening, reduced inflammation, creatine kinase isoenzyme (CK)-MB, and lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) levels decreased, while interferon-γ and interleukin-6 (IL-6) increased, and the M2/M1 cell ratio was upregulated. In conclusion, miR-19b-3p can regulate macrophage polarization by targeting PKNOX1, and has a protective effect against CVB3-induced inflammation and myocardial injury.
研究领域:
分子生物学
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心脏病学
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病毒学
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免疫学
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产品关联
DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2025
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IF 4.2
Xiaoqi Wang,Shuang Liu,Di Su,Jiayu Sui,Xiangyu Yan,Jia Yang,Ziqi Zheng,Penghe Wang,Weijun Song,Zexi Jin,Mingyan E,Maomao Zhang,Bo Yu
Background and aims Viral myocarditis is an inflammatory pathology of the myocardium that involves innate immune responses, especially those involving neutrophils. However, strategies targeting neutrophils to alleviate inflammation have not achieved complete success. Alpha lipoic acid (ALA), a natural organosulfur compound, has the capacity to modulate immune cell behavior. This study aimed to investigate whether ALAs can regulate innate immunity to provide protection against coxsackievirus B3 (CVB3)-induced myocarditis. Methods and results Abdominal administration of ALA improved cardiac dysfunction and reduced mortality in a CVB3-induced mouse model of myocarditis (VM). ALA treatment induced neutrophils and inhibited Ly6C hi pro-inflammatory macrophages, favoring a reparatory environment in the myocardium. However, depleting neutrophils with anti-Ly6G antibodies increased Ly6C hi pro-inflammatory macrophage recruitment in blood and heart in ALA-treated VM mice. Further flow cytometry analysis indicated that ALA promoted Ym-1 expression of neutrophils. Blocking Ym-1 significantly reversed ALA-mediated cardiac reparative macrophages infiltration and cardiac function improvement post-VM. Recombinant Ym-1 drives macrophages toward a reparative phenotype and attenuates CVB3-induced viral myocarditis. Mechanistically, ALA reprogrammed neutrophil metabolic patterns, leading to increased production of the metabolite acetyl-CoA, thereby increasing the transcription of Ym-1 by promoting STAT6 acetylation. Conclusions ALA protects against VM by activating metabolic reprogramming/STAT6 acetylation/Ym-1 axis in neutrophils. These results highlight the heterogeneity of neutrophils and suggest that ALA might represent a feasible strategy to improve the prognosis of VM patients.
研究领域:
免疫学
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病毒学
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心脏病学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2024
·
IF 7.7
Changwei Zhang,Qinghui Cao,Yuanyu Li,Juan Lu,Sidong Xiong,Yan Yue
The induction of a robust CD8 + T cell response is critical for the success of an antiviral vaccine. In this study, we incorporated a STING agonist (SA) 2′3’-cGAMP into a previously developed exosome-based CVB3 viral myocarditis vaccine (Exo-VP1) to enhance its ability to induce CD8 + T cell responses and immunoprotection. Our results showed that compared to free SA adjuvant, exosome-mediated co-delivery (Exo SA -VP1) significantly enhanced SA uptake by dendritic cells (DCs) and more potently stimulated DC maturation. Immunization of mice showed that the Exo SA -VP1 vaccine-induced higher levels of CVB3-specific T cell proliferation and cytotoxicity, significantly increased the percentage of IFN-γ + CD8 + rather than CD4 + T cells, effectively reduced cardiac viral loads, attenuated myocarditis and improved survival in mice compared to the previous Exo-VP1 vaccine. Further investigation showed that Exo SA -VP1 significantly increased both the percentage and antigen cross-presentation capacity of splenic CD8 + DCs. Depletion of these CD8 + DCs by cytochrome C administration nearly abolished the advantage of Exo SA -VP1 in dominantly inducing IFN-γ + CD8 + cytotoxic T lymphocyte (CTL) production in immunized mice. Taken together, our results demonstrated the potential of Exo SA -VP1 as a promising candidate for anti-CVB3 vaccines and provide insights into immune-enhancing strategies aiming at augmenting antigen cross-presentation by DCs and enhancing potent CTL responses.
研究领域:
免疫学
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病毒学
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药学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Small
·
2021
·Vol. 17
·期 44
·2103627
·
IF 13.281
Linyao Li,Peilin Gu,Mengqi Hao,Xiaoli Xiang,Yuting Feng,Xiaokang Zhu,Yang Song,Erqun Song
Despite the significant advances of imaging techniques nowadays, accurate diagnosis of bacterial infections and real-time monitoring the efficacy of antibiotic therapy in vivo still remain huge challenges. Herein, a self-assembling peptide (FFYEGK) and vancomycin ( Van ) antibiotic molecule co-modified gadolinium (Gd) MRI nanoaggregate probe (GFV) for detecting Staphylococcus aureus ( S. aureus ) infection in vivo and monitoring the treatment of S. aureus- infected myositis by using daptomycin ( Dap ) antibiotic as model are designed and fabricated. The as-prepared GFV probe bears Van molecules, making itself good bacteria-specific targeting, and the peptide in the probe can enhance the longitudinal relaxivity rate ( r 1 ) after self-assembly due to the π–π stacking. The study showed that, based on the GFV probe, bacterial infections and sterile inflammation can be discriminated, and as few as 10 5 cfu S. aureus can be detected in vivo with high specificity and accurately. Moreover, the T 1 signal of GFV probe at the S. aureus -infected site in mice correlates with the increasing time of Dap treating, indicating the possibility of monitoring the efficacy of antibacterial agents for infected mice based on the as proposed GFV probe. This study shows the potential of GFV probe for diagnosis, evaluation, and prognosis of infectious diseases in clinics.
研究领域:
医学成像
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微生物学
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药理学
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纳米技术
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
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2025
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IF 11.5
Zhou Ye,Manman Zhu,Shaojie Li,Fan Zhang,Yingqi Ran,Cong Liu,Xiangchang Xu,Shujiao Liu,Xiang Xie,Yingchen Wang,Lan Yao
Cardiac autoimmune injury and oxidative stress play critical roles in the development of myocarditis. Promising approaches for treating this condition include suppressing excessive immune responses and reducing oxidative stress in the myocardium. The programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) axis is known to regulate immune responses and prevent damage caused by T-cell overactivation, while elevated reactive oxygen species (ROS) contribute to the progression of myocarditis. In this study, we developed multifunctional nanoparticles (PMN@EDR) that overexpress PD-L1 and are loaded with edaravone (EDR). The PMN@EDR NPs were successfully synthesized and comprehensively characterized. PMN@EDR effectively targeted inflammation-stimulated CD4 + T cells and damaged myocardial cells, inhibiting CD4 + T-cell proliferation, activation, and the release of pro-inflammatory cytokines via the PD-1/PD-L1 pathway. Additionally, PMN@EDR further suppressed CD4 + T-cell activation and alleviated HL-1 cardiomyocyte damage by releasing EDR to eliminate free radicals. For the in vivo treatment of myocarditis, compared to traditional single-target anti-inflammatory and antioxidant drugs, PMN@EDR not only reduced inflammation and the release of inflammatory mediators but also decreased ROS levels, thereby minimizing cardiomyocyte apoptosis and improving cardiac function. In conclusion, the PMN@EDR-based modulation of immune responses and oxidative stress offers a promising therapeutic strategy for myocarditis.
研究领域:
纳米技术
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免疫学
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心脏病学
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药理学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Huizhen Tian,Qigang Pan,Jianfeng Wu,Juanjuan Liao,Yuwei Wan,Ke Pei,Qiong Liu,Lingbing Zeng,Yanli Cao,Qiaofa shi,Nanzhen Kuang,LiJuan Sun,Xiaomin Yu,Xiaotian Huang
Background Coxsackievirus B3 (CVB3) is a leading cause of viral myocarditis and is currently lacking specific pharmacological treatments, highlighting the critical need for therapeutic development. Icariin (ICA), a prenylated flavonol glycoside, was previously found to exhibit several pharmacological effects, but its potential to combat CVB3 remains uninvestigated. Purpose This study aimed to elucidate the anti-CVB3 efficacy of ICA and elucidate its molecular mechanisms. Methods CVB3-infected HeLa cells, H9C2 cells and neonate rat ventricular cardiomyocytes (NRVCs) were selected as in vitro models, and were treated with ICA at 1 and 10 μM. Additionally, BALB/c mice that were infected with CVB3 via intraperitoneal injection were chosen as in vivo model and were treated with ICA or ribavirin over 3 days. The effect of ICA against CVB3 was determined by Cell Counting Kit-8 (CCK-8) assay, western blot, real-time fluorescence quantitative PCR (RT–qPCR), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, hematoxylin and eosin (H&E) staining, immunohistochemistry (IHC) and flow cytometry. Results In this study, it was found that ICA is capable of reducing CVB3 viral load both in vitro and in vivo . Mechanistic studies suggested that ICA prevents cardiomyocyte apoptosis by attenuating the S100 calcium binding protein A6 (S100A6)/β-catenin/c-Myc signaling pathway. Additionally, ICA inhibits the secretion of proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1beta (IL-1β) and CXC motif chemokine ligand 2 (CXCL2) in heart tissue, thereby mitigating CVB3-induced myocarditis. Moreover, ICA also regulates the immune response of CD4 + T, CD8 + T and Treg cells by changing the cells numbers in spleen tissue. Lastly, ICA can reduce the load of other enteroviruses (such as CVA6, CVA16 and EV71) in rhabdomyosarcoma (RD) cells as well. Conclusion Our findings indicate that ICA provides significant protection against CVB3 infection by modulating the S100A6/β-catenin/c-Myc signaling pathway, suggesting its potential use as a novel drug against CVB3 infection in clinical application.
研究领域:
药理学
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病毒学
·
心脏病学
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免疫学
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细胞生物学
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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）