ENVIRONMENT INTERNATIONAL
·
2024
·
IF 10.3
Bilin Zhao,Shuang Zheng,Gaoxiang Yang,Zhijun He,Jiewei Deng,Lijuan Luo,Xinyan Li,Tiangang Luan
Aryl organophosphorus flame retardants (aryl-OPFRs), commonly used product additives with close ties to daily life, have been regrettably characterized by multiple well-defined toxicity risks. Triphenyl phosphate (TPHP) and tri-o-cresyl phosphate (TOCP), two structurally similar aryl-OPFRs, were observed in our previous study to exhibit contrasting immunotoxic effects on THP-1 macrophages, yet the underlying mechanisms remain unclear. This study sought to address the knowledge gap by integrating transcriptomic and metabolomic analyses to elucidate the intricate mechanisms. During individual omics analyses, we unfortunately only obtained highly similar results for both TPHP and TOCP, failing to identify the key reasons for their differences. These results revealed comparable disturbances induced by both compounds, including disruptions in nucleic acid synthesis and energy metabolism, blocking ADP to ATP conversion by reducing TCA cycle intermediates, consequently leading to ATP depletion. However, through integrative analysis, specific pathways affected by each compound were successfully identified, shedding light on their unique effects. TPHP reduced GTP levels necessary for Rap1 activation, thereby inhibiting phagocytosis and adhesion of THP-1 macrophages. Conversely, TOCP stimulated the mTOR signaling pathway, enhancing phosphorylation of downstream proteins S6K, RHOA, and PKC, consequently promoting immune responses. This study not only clarified the distinct immunotoxic mechanisms of TPHP and TOCP but also provided critical insights into how structural variations in aryl-OPFRs can lead to markedly different immune responses, thereby informing future risk assessments and regulatory strategies for these compounds.
研究领域:
毒理学
·
免疫学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2025
·
IF 4.8
Zibo Li,Ziyang Huang,Zhiyi Wang,Zhenzhen Guo,Baoying Wang,Yucheng Li,Erping Xu
Background: Chaihu Longgu Muli Decoction (CLM) is a classical herbal formula originally documented in Shang Han Lun. With an 1800-year clinical history, CLM remains widely prescribed for depression (“Yu Zheng” in Traditional Chinese Medicine theory). Emerging evidence suggests that chronic stress-induced depression is closely linked to lung cancer progression and metastasis. However, the therapeutic potential of CLM in this context remains unexplored.Methods: A lung cancer cell xenograft model combined with chronic unpredictable mild stress (CUMS) was used to evaluate the effect of CLM on lung cancer growth. Proteomic analysis was performed to explore the underlying mechanisms by which CLM alleviates CUMS-induced lung cancer progression. Western blot and qPCR were conducted to detect changes in Rap1/ERK-mediated epithelial-mesenchymal transition (EMT) progression. Finally, Rap1 agonists were utilized to determine the therapeutic mechanism of CLM on cortisol or corticosterone (Cort)-induced EMT progression in lung cancer cells and a mouse lung cancer model.Results: In our study, CUMS promoted lung cancer xenograft growth, increased the expression of the proliferation marker Ki67, and elevated serum Cort levels. CLM treatment not only alleviated CUMS-induced depression-like behaviors, but also suppressed stress-driven tumor growth. These effects were replicated in a urethane-induced lung cancer model combined with CUMS. Proteomic analysis revealed that CLM’s anti-tumor effects were associated with modulation of the Rap1 pathway. Mechanistically, CUMS downregulated Rap1GAP, activating Rap1 and subsequent ERK1/2 phosphorylation, thereby promoting EMT in lung cancer tissues. CLM effectively reversed these effects by inhibiting Rap1/ERK-mediated EMT. In vitro, CLM suppressed cortisol-induced migration, invasion, and EMT in lung cancer cells, and these effects were attenuated by Rap1 agonists. Furthermore, CLM inhibited Cort-induced EMT and depression-like behaviors in vivo, while Rap1 activation diminished CLM’s efficacy against Cort-driven tumor growth.Conclusion: These findings suggest that Rap1/ERK-mediated EMT is a hallmark of chronic stress-associated lung cancer progression. CLM exerts its therapeutic effects by targeting this pathway, offering a novel strategy to mitigate stress-aggravated oncogenesis.
研究领域:
肿瘤学
·
分子生物学
·
药理学
·
应激与疾病
·
转化医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Biomaterials Advances
·
2025
·
IF 6
Ying Sun,Yining Cai,Shanshan Xu,Ningning Zhai,Zirui Wang,Zongpu Qiu,Shuying Han,Yuanqing Wei,Rui Liu,Hao Wu
While the regulatory roles of biomaterial topology in bone regeneration are recognized, the specific osteogenic mechanisms driven by distinct morphological features, particularly without biochemical cues, remain poorly understood. This study aimed to independently elucidate the osteogenic potential and underlying mechanisms solely attributable to the distinctive “S”-grooved topology derived from cuttlebone. Inspired by cuttlebone, we successfully fabricated a biomimetic polycaprolactone (PCL) membranes sheet with “S”-grooved topology using liquid silicone mold replication combined with PCL recasting techniques. Comprehensive characterization (SEM, CLSM) confirmed precise replication of the native “S”-grooved morphology (width: 100 ± 30 μm, depth: 20 ± 6 μm). In vitro studies revealed that these grooves promoted directional adhesion and proliferation of rat bone marrow mesenchymal stem cells (rBMSCs) via contact guidance, as evidenced by cytoskeleton alignment. Furthermore, the “S”-grooved topology significantly enhanced osteogenic differentiation of mouse pre-osteoblasts (MC3T3-E1), demonstrated by increased alkaline phosphatase (ALP) activity and mineralized nodule formation. Mechanistic investigations using RT-qPCR, Western blot, and dimethyl labeling-based quantitative proteomics on rBMSCs identified key involvement of the Rap1-ERK signaling pathway. Specifically, the “S”-grooved topology upregulated Rap1 expression and enhanced ERK phosphorylation, leading to increased expression of osteogenic markers (e.g., Runx2, OPN). These findings demonstrate that the biomimetic “S”-grooved topology alone, through contact guidance and activation of the Rap1-ERK mechanotransduction pathway, significantly enhances osteogenic differentiation, providing a foundation for designing topologically optimized biomaterials for bone regeneration biomimetic PCL membranes sheet with the “S”-grooved topology.
研究领域:
生物材料
·
组织工程
·
细胞生物学
·
生物医学工程
·
材料科学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Cell Death & Disease
·
2018
·Vol. 9
·期 3
·1-15
·
IF 5.638
Ding Yue,Liang Xiaoting,Zhang Yuelin,Yi Li,Shum Ho Cheung,Chen Qiulan,Chan Barbara P.,Fan Huimin,Liu Zhongmin,Tergaonkar Vinay,Qi Zhongquan,Tse Hung-fat,Lian Qizhou
Immunomodulatory activity of mesenchymal stem cells (MSCs) is largely mediated by paracrine factors. Our previous studies showed that activation of nuclear factor-kappa B (NF-κB) regulates cytokine/growth factor secretion by MSCs. This study aimed to elucidate the role of Rap1 (repressor/activator protein), a novel modulator involved in the NF-κB pathway, in regulating the immunomodulatory potency of MSCs in acute allograft rejection of heart transplantation. The immunosuppressive potency of wild-type MSCs (WT-MSCs) or Rap1-deficient MSCs (Rap1 −/− -MSCs) was examined in mice with acute allograft rejection following heart transplantation. With a combination of immunosuppressant rapamycin at a dose of 1 mg/kg/d, WT-MSCs notably prolonged the survival of the transplanted heart compared with Rap1 −/− -MSCs. Rap1 −/− -MSCs displayed a marked insensitivity to inhibit the mixed lymphocyte reaction (MLR) due to impaired cytokine production and a significantly reduced activity of NF-κB signaling in vitro . Finally, transplantation of encapsulated WT-MSCs greatly prolonged the survival of the heart allograft compared with encapsulated Rap1 −/− -MSCs. Our results indicate that Rap1 is essential to maintain the immunomodulatory function of MSCs. Deletion of Rap1 results in impaired immunomodulatory function of MSCs.
研究领域:
免疫学
·
干细胞研究
·
移植医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Chinese Medicine
·
2024
·Vol. 19
·期 1
·1-17
·
IF 5.3
Gao Jiaming,Guo Hao,Li Junmei,Zhan Min,You Yue,Xin Gaojie,Liu Zixin,Fan Xiaodi,Gao Qinghe,Liu Jianxun,Zhang Yehao,Fu Jianhua
Background Buyang Huanwu Decoction (BYHWD) is a traditional Chinese medicine to treat the syndrome of qi deficiency and blood stasis. Platelets play an important role in regulating thrombus and inflammation after ischemic injury, studies have shown that BYHWD regulate myocardial fibrosis and exert anti-inflammatory effects through IL-17 and TLR4 pathways, but the mechanism of platelet activation by BYHWD in stable coronary heart disease is still unknown. In the present study, model of left anterior descending coronary artery ligation was applied to investigate the mechanisms of BYHWD on modulating platelets hyperreactivity and heart function after fibrosis of ischemic myocardial infarction (MI). Methods Myocardial infarction model was constructed by ligation of the left anterior descending coronary artery. The rats were randomly divided into five groups: sham, model, MI with aspirin (positive), MI with a low dosage of BYHWD (BYHWD-ld) and MI with a high dosage of BYHWD (BYHWD-hd) for 28 days. Results Coronary artery ligation prominently induced left ventricle dysfunction, increased cardiomyocyte fibrosis, which was accompanied by platelets with hyperreactivity, and high levels of inflammatory factors. BYHWD obviously reversed cardiac dysfunction and fibrosis, increased the thickness of the left ventricular wall, and inhibited aggregation ratio and CD62p expression. BYHWD restored the mitochondrial respiration of platelets after MI, concomitant with an increased telomere expression and decreased inflammation. According to the result of transcriptome sequencing, we found that 106 differentially expressed genes compared model with BYHWD treatment. Enrichment analysis screened out the Ras-related protein Rap-1 (Rap1) signaling pathway and platelet activation biological function. Quantitative real-time PCR and Western blotting were applied to found that BYHWD reduced the expression of Rap1/PI3K-Akt/Src-CDC42 genes and attenuated the overactivity of PI3 kinase/Rap1/integrin α(IIb)β(3) pathway. Conclusion BYHWD reduced inflammation and platelet activation via the PI3 kinase/Rap1/integrin α(IIb)β(3) pathway and improved heart function after MI. Graphical Abstract
研究领域:
中医
·
心脏病学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Translational Medicine
·
2025
·Vol. 23
·期 1
·1-18
·
IF 7.5
Tan Yanzhen,Li Hong,Cao Guojie,Xin Jialin,Yan Dongxu,Liu Yingying,Li Panpan,Zhang Yuxi,Shi Lei,Zhang Bing,Yi Wei,Sun Yang
Background In developed nations, myocardial infarction (MI) is one of the main causes of morbidity and mortality, resulting in a significant economic burden and becoming a global public health problem. C1q/tumor necrosis factor-related protein 9 (CTRP9) is a secreted protein comprising a variable domain, a collagenous region, and a C-terminal trimerizing globular C1q (gC1q) domain. In vivo, the full-length CTRP9 (fCTRP9) can be cleaved into the globular domain of CTRP9 (gCTRP9). Here, we tested the cardio-protective impacts of fCTRP9, gCTRP9, and N-terminal domain, including the variable and collagenous domain, of CTRP9 (nCTRP9) in the context of MI.Methods Studies comparing the protective properties of fCTRP9 and gCTRP9 against MI in mice hearts were performed both in vitro and in vivo. The role of matrix metalloproteinase-9 (MMP9) in CTRP9 cleavage was examined, and the effects of different CTRP9 domains on cardiac fibrosis and cardiac fibroblast (CF) activation were investigated.Results gCTRP9 exerted better protective effects than fCTRP9 against MI, demonstrating superior anti-apoptotic and anti-fibrotic properties. fCTRP9 was cleaved by MMP9, resulting in gCTRP9 and nCTRP9. MMP9 overexpression enhanced the cardioprotective effects of fCTRP9, while nCTRP9 supplementation aggravated cardiac fibrosis in MI mice. Mechanistically, nCTRP9 activated CFs via an increase in Rap1 expression and MEK 1/2 and ERK1/2 phosphorylation.Conclusion sDifferent domains of CTRP9 have distinct cardioprotective effects. gCTRP9 shows beneficial effects, while nCTRP9 promotes cardiac fibrosis. These findings highlight the importance of CTRP9 in cardiac function regulation and suggest prospective therapeutic options for MI treatment.
研究领域:
心脏病学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Bioscience-Landmark
·
2024
·Vol. 29
·期 9
·325
·
IF 3.3
Ziwei Guo,Sixu Bao,Zehui Shi,Xuejiao Li,Peijin Li,Bin Zhong,Ming Zhang,Qiyong Wu
Background: Platelets have the hemostatic function, and their aberrant activation is associated with occlusive thrombus formation. Plasma exosomes are rich in platelets containing ubiquitin-specific peptidase 15 (USP15). Herein, we aim to explore the effect of USP15 on thrombosis, as well as expounding whether USP15 acts as an upstream target of FK506 binding protein 5 (FKBP5) to regulate occlusive thrombus formation. Methods: Washed human platelets were treated with thrombin for measurement of USP15 and FKBP5 expressions. USP15 loss/gain-of-function variant in HEK293 cells was performed by cell transfection, and the interaction between USP15 and FKBP5 was examined using immunoprecipitation and ubiquitination assays. Mice with USP15-knockout platelets (Plt USP15-/-) were modeled, and subjected to calculation of bleeding time, artery thrombosis imaging and clot retraction assay. FKBP5 expression and the inhibitor of nuclear factor kappa B kinase subunit epsilon (IKBKE)/phosphatidylinositol 3-kinase (PI3K)/Rap1 pathway in wild-type and Plt USP15-/- mice-derived platelets were detected using Western blot. The activation of αIIbβ3 in washed platelets was analyzed using flow cytometry. Results: USP15 and FKBP5 expressions were upregulated in platelets after thrombin treatment. Following transfection of USP15 knockdown and USP15 overexpression plasmids into HEK293 cells, FKBP5 protein expression was downregulated by USP15 knockdown while being upregulated by USP15 overexpression. USP15 bound to FKBP5 and protected FKBP5 against ubiquitination. Knockdown of platelet USP15 prolonged bleeding time, inhibited arterial thrombosis and delayed clot retraction in mice. Knockdown of platelet USP15 also decreased protein expressions of FKBP5, IKBKE and Rap1, p-PI3K/PI3K ratio, and activation of αIIbβ3 in mice. Conclusion: USP15 knockdown in platelets affects thrombosis in mice by promoting the instability of FKBP5 to repress the activation of IKBKE/PI3K/Rap1 pathway-mediated αIIbβ3.
研究领域:
血液学
·
分子生物学
·
血栓
·
细胞信号传导
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Bioactive Materials
·
2025
·
IF 20.3
Xiaoqian Lan,Guangli Feng,Qing Li,Shiyi Qin,Yingrui Hu,Shilin Pan,Jianlin Jiao,Di Lu,Lianmei Zhong
Peripheral nerve injuries tend to cause the proximal nerve unable to contact the corresponding target organ, resulting in sensory and motor dysfunction. The simple filling materials within nerve conduits are often inadequate for axonal ingrowth and directional regeneration. In this study, to enhance the guidance effect and achieve physiologically adaptive function, a 3D nanofibrous polyurethane (PU) scaffold with oriented microchannels was engineered using electrospinning and manual curling techniques. The electrospun fibrous membranes can be manually curled up into tubular structures with spiral and longitudinal multi-channels. The immunoregulatory and conductive properties were developed by being grafted gastrodin and aniline trimer (AT, 2.6 % and 5 %). Gastrodin stimulated proliferation of neural cells and expression of neuroblast-related genes. Electroactive AT produced an electrical signal in combination with electrical stimulation (ES) to accelerate the elongation and growth of Schwann cells (SCs) and neurite outgrowth of PC12 cells. The in vivo experiments revealed that the releasing gastrodin and electrical signals created prohealing microenvironment for alleviating inflammation and promoting vascularization. Of note, the topological structure provided well-organized internal support for the cells to spread, as well as the migration of SCs and the directional elongation of regenerating axons. The adaptive electroactivity of gastrodin-PU-AT5 % further ensured nerve signal transmission, ultimately promoted remyelination through upregulation of Rap1 and mTOR signaling pathways; thereby enhancing functional and structural regeneration. This scaffold design strategy will push forward the application of nerve conduits in long-distance peripheral nerve injury.
研究领域:
生物医学工程
·
神经组织工程
·
再生医学
·
生物材料
·
神经科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Diabetes Metabolic Syndrome and Obesity-Targets and Therapy
·
2025
·
IF 3
Shizhao Zhang,Mei Yan,Pengpeng Liang,Ye Zhang,Jiamin Liu,Hai Huang,Guiyun Li,Hongyan Wu
Objective This study aimed to investigate the active ingredients and mechanisms of Fu-Fang-Qi-Di-Hua-Yu-Tang (FFQD) in alleviating atherosclerosis and insulin resistance in diabetic macrovascular disease (DMD) mice.Methods Chemical profiling of FFQD was performed using UPLC-Q-TOF-MS. Apoe-/- mice were injected with streptozotocin and fed a high-fat diet to establish DMD. Groups included control (C57BL/6), model (normal saline), low/medium/high-dose FFQD, and western medicine (atorvastatin + metformin). After 12 weeks, aortic morphology, blood glucose/lipid profiles, inflammatory factors, and PI3K/AKT pathway-related targets were analyzed.Results FFQD contained 159 identified components. Treatment significantly reduced aortic plaque area, blood glucose, lipids, and lowered the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), oxidized low-density lipoprotein (ox-LDL), C-reactive protein (CRP), and monocyte chemoattractant protein-1 (MCP-1). It also reduced nitric oxide synthase 2 (NOS2) level, a marker of macrophage polarization, increased arginase 1 (Arg1) level, regulated macrophage polarization, and improved oxidative stress and inflammatory response. In addition, FFQD activated the receptor for advanced glycation end products (RAGE)/PI3K/AKT/mammalian target of rapamycin (mTOR) pathway in the aorta, inhibited RAGE expression, promoted PI3K, AKT, and mTOR phosphorylation, down-regulated microtubule-associated protein 1A/1B-light chain 3-II/I (LC3 II/I) and nuclear factor κB (NF-κB p65) expression, up-regulated SQSTM1 protein (p62) expression, inhibited excessive autophagy, and reduced vascular endothelial damage caused by long-term high glucose levels. In the liver, FFQD activated the Ras family small molecule G protein (RAP1)/PI3K/AKT/forkhead box protein 01 (FOX01) pathway, inhibited RAP1 expression, promoted PI3K and AKT phosphorylation, suppressed FOX01 expression, and improved insulin resistance.Conclusion FFQD may improve insulin resistance, regulate glucose and lipid metabolism, inhibit excessive autophagy, induce macrophage polarization, resist inflammation and oxidative stress, inhibit atherosclerosis, and ultimately improve DMD by activating the RAGE/PI3K/AKT/mTOR and RAP1/PI3K/AKT/FOX01 pathways. Therefore, FFQD may be a promising candidate for DMD treatment.
研究领域:
药理学
·
中医药学
·
心血管疾病
·
分子生物学
·
代谢紊乱
·
免疫学
·
病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2022
·
IF 5.195
Jinfeng Shang,Qiannan Li,Tingyue Jiang,Lei Bi,Yinghui Lu,Jiakang Jiao,Qi Song,Mingxue Yan,Lizha Shabuerjiang,Jingyi Wang,Xin Liu
Ethnopharmacological relevance Huanglian Jiedu Decoction (HLJDD) has the effect of clearing heat and detoxifying, and has been considered as an effective prescription for cerebral ischemia (CI) for thousands of years in traditional Chinese medicine (TCM). It can improve the quality of life of patients with ischemic stroke, but its pharmacological mechanism remains unclear. Aim of the study The study aimed to explore the pharmacological action and potential mechanism of HLJDD against CI by systems pharmacology, proteomics and in vivo experiments. Materials and methods In this study, databases such as TCMIP V2.0 and Genecards were used to predict compounds, targets and CI related targets, and network topology criteria of protein-protein interaction (PPI) network was used to screen core targets. The Database for Annotation, Visualization and Integrated Discovery database (DAVID) was used to discover biological processes and pathways. In addition, molecular docking was performed between the screened core biological active compounds and targets to verify the binding activity. Finally, proteomics and Western blot were performed on cerebral cortex tissues of middle cerebral artery occlusion (MCAO) model rats with HLJDD intervention to further verify the predicted results. Results 77 compounds and 308 targets of HLJDD were identified, 54 of which were predicted to be associated with cerebral ischemia. PPI network and enrichment results showed that 8 targets, including AKT1, PTGS2 and TLR4 , were core targets of HLJDD in CI. And 19 signaling pathways, including Rap1 signaling pathway, cAMP signaling pathway and arachidonic acid metabolism, were identified as key pathways to the therapeutic activity of HLJDD in CI. Combined with proteomics studies, we identified that Rap1 signaling pathway and upstream and downstream targets were the key mechanisms. Molecular biology experiments showed that RAP1A and AKT expression levels were significantly up-regulated in middle cerebral artery occlusion (MCAO) rats treated with HLJDD ( P < 0.0001), GRIN1 expression level was significantly down-regulated ( P < 0.0001). However, ACTB expression level was slightly down-regulated ( P > 0.05), which may be related to the biological function. Conclusion This study confirms the pharmacological effect of HLJDD on cerebral ischemia. These results indicate that HLJDD mediates various pathways such as inhibition of apoptosis , regulation of oxygen balance, inhibition of excitatory toxicity and maintenance of basic cell functions to improve CI by regulating Rap1 signaling pathway.
研究领域:
药理学
·
神经科学
·
中医
·
分子生物学
·
生物信息学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2024
·
IF 13.3
Ye Liu,Sicheng Li,Jinjian Huang,Xuanheng Li,Ze Li,Canwen Chen,Guiwen Qu,Kang Chen,Yitian Teng,Rui Ma,Xiuwen Wu,Jianan Ren
Open abdomen (OA), a major advance in modern trauma surgery, enables the treatment of severe abdominal trauma, infections, and hypertension by temporarily closing the abdominal cavity without suturing. Although OA can reduce mortality rates, it also presents challenges such as disruption of the abdominal environment, intestinal exposure, and impaired wound healing. Current temporary abdominal closure (TAC) techniques using polypropylene (PP) mesh are susceptible to abrasion and rupture of the intestine, leading to adhesions and serious complications such as intestinal fistulas and chronic wounds. These complications seriously impact outcomes due to mesh rigidity and its incompatibility with surrounding tissues. In this study, we designed a multifunctional hydrogel composed of GelMA (Gelatin Methacryloyl) and SilMA (Silk Fibroin Methacryloyl) as a promising solution for open abdominal wound repair. In vitro experiments confirmed the biocompatibility, self-healing properties, pro-angiogenic effects, and promotion of macrophage polarization. In vivo studies revealed that the GelMA-SilMA hydrogel could enhance abdominal wall tissue thickness and integrity via isolating the peritoneal cavity, protecting the intestinal tract, polarizing macrophages, promoting collagen formation, inducing neovascularization, inhibiting oxidative stress, and suppressing inflammation. Furthermore, immunofluorescence, immunohistochemistry, and RNA sequencing were employed to evaluate the wound healing mechanisms of GelMA-SilMA hydrogels. The results demonstrated that the hydrogels can promote angiogenesis, inhibit inflammation and immune responses, and enhance wound healing by activating the HIF-a-VEGF signaling pathway, RAP1 signaling pathway, and PI3K-AKT signaling pathway. Hence, the multifunctional GelMA-SilMA hydrogel has tremendous potential for clinical use in open abdominal wound repair.
研究领域:
生物医学工程
·
组织工程
·
伤口愈合
·
材料科学
·
外科技术
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）