Nature Communications
·
2026
·
IF 18.1
Li Chao,Chen Zehao,Li Wentao,Deng Ronghui,Huang Lingan,Song Yifan,Wang Yiqun,Cui Guoqing,Liu Huawei,Yu Jiakuo
Excessive transforming growth factor-β1 (TGF-β1) signaling is a key driver of the pathological processes of fibrosis and matrix disorganization in tendinopathy, yet current treatments do not directly target this fibrotic microenvironment. Here we show that a self-assembling peptide composed entirely of natural amino acids, AsPep-FTSQ, can locally capture TGF-β1 and remodel the pathological tendon niche. Injecting AsPep-FTSQ into rat and beagle models of tendinopathy resulted in the formation of an interconnected nanofibrous network in situ that selectively sequesters excess TGF-β1. This network suppresses pro-fibrotic signaling, limits pathological tendon cell (TC) state transitions, and promotes collagen realignment. These effects improve tendon structure and functional repair across species. This fully natural, self-assembling peptide composed of amino acids provides a modular strategy for local cytokine sequestration and suggests a therapeutic approach for tendinopathy and potentially other fibrotic soft-tissue disorders.
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高影响因子
Frontiers of Medicine
·
2025
·
IF 3.5
Li Fengchan,Ni Haofu,Tang Fan,Lyu Jiaxin,Wu Lili,Ren Lijie,Lu Qiongyu,Zhao Shouming,Tang Chaojun,Zhu Li
Atherosclerosis is a chronic inflammatory disease driven by pathological processes such as macrophage foam cell formation. Semaphorin 7A (SEMA7A) is an immunoregulatory signaling molecule known to modulate immune responses and cellular adhesion. However, the contribution of macrophage-derived SEMA7A to atherogenesis has yet to be fully elucidated. In this study, we analyzed gene expression profiles of human mononuclear cells from the Gene Expression Omnibus (GEO) database and revealed highly expressed SEMA7A and its receptor integrin β1 in macrophages. The upregulation of SEMA7A and integrin β1 was also observed during the differentiation of THP-1 monocytes into macrophages. Mice with macrophage-specific deletion of Sema7a showed a 57.2% reduction in atherosclerotic lesion size and improved plaque stability in atherosclerosis mouse model compared to control mice. Mechanistically, macrophage SEMA7A promoted the expression of macrophage scavenger receptor 1 (MSR1) and lipid uptake mediated by integrin β1 and downstream JNK signaling pathway in macrophages. Notably, pharmacological inhibition of integrin β1 with integrin receptor antagonist GLPG0187 effectively suppressed atherosclerosis progression. These findings identify macrophage-derived SEMA7A as a key driver of atherosclerosis through a novel integrin β1/JNK/MSR1 axis, providing potential targets for the prevention and treatment of atherosclerosis.
研究领域:
心血管研究
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免疫学
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分子生物学
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炎症
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PubMed
高影响因子
BIOLOGY OF REPRODUCTION
·
2025
·Vol. 114
·期 3
·871-882
·
IF 3
Yang Jinjin,Ren Li,Gu Xiaoli,Wang Lu,Cui Jinquan
Intrauterine adhesion (IUA) is an adhesion of the uterine cavity or cervical canal resulting from damage to the basal layer of the endometrium， usually accompanied by fibrosis of the endometrium. This study analyzed endometrial samples from three IUA patients and three healthy control participants and screened for differentially expressed genes (DEGs) using RNA-seq and bioinformatics techniques. A total of 2402 DEGs were identified in endometrial tissues compared to normal endometrial tissues, among which microfibrillar-associated protein 5 (MFAP5) was upregulated in IUA tissues (log2FoldChange = 3.81, P = 1.98E-08). Meanwhile, clinical tissue specimens revealed remarkably up-regulated MFAP5 expression in endometrial tissues of IUA patients, accompanied by increases in the fibrosis markers collagen type I A 1 and α-smooth muscle actin. A mouse model of IUA was constructed by mechanical curettage. Histopathology revealed that MFAP5 downregulation attenuated IUA model-induced reduction in endometrial gland number and collagen deposition. Furthermore, MFAP5 knockdown alleviated the increase in embryo uptake ratio and the decrease in embryo and placental weight in IUA model. In vitro, the expression of fibrosis indicators was upregulated in Ishikawa cells treated with 5 ng/mL transforming growth factor-β1 (TGF-β1), while MFAP5 siRNA reduced levels of the endometrial fibrosis markers. RNA-seq analysis was performed on normal-treated and MFAP5 knockdown-treated TGF-β1-induced cell lines. Enrichment analysis revealed that the MFAP5 siRNA may be involved in microfibril formation, collagen deposition, and the TGF-β pathway. These results further confirm the potential role of MFAP5 in promoting endometrial fibrosis, which provides new insight for the clinical treatment of IUA.
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高影响因子
Frontiers in Immunology
·
2026
·
IF 5.9
Xifan Zheng,Bo Yu,Yuansong Song,Yeping Chen,Zeming Li,Jun Yao
Objective Osteoarthritis (OA) involves an inflammatory imbalance, yet key mediators and their interplay with potential therapeutics like artemisinin (ART) remain poorly understood. This study aimed to systematically investigate these relationships using Mendelian randomization and to decipher their functional interactions through cellular and molecular experiments, complemented by network pharmacology and molecular docking analyses. Methods Using the Mendelian randomization (MR) method, we integrated independent exposure–outcome genome-wide association study data to evaluate the causal association between inflammatory cytokines and OA. Chondrocytes were treated with IL-1β, TGF-β1 (5 μg/mL), and ART (4 μg/mL) for 24 hours. Cell proliferation was assessed using CCK-8 and EdU assays, and gene/protein expression was analyzed via RT-qPCR, Western blotting, and immunofluorescence staining. In parallel, network pharmacology was performed to identify putative ART targets related to OA and to characterize enriched pathways and hub genes through GO/KEGG enrichment and protein–protein interaction (PPI) analyses. Molecular docking was further conducted to evaluate the binding feasibility between ART and the catabolic mediator MMP-13. Results MR revealed a positive association between TGF-β1 and OA risk (OR = 1.0526, P = 0.0182). Functionally, ART significantly enhanced chondrocyte proliferation, whereas TGF-β1 inhibited it. ART downregulated IL-1β and MMP13 expression, while TGF-β1 upregulated them, indicating opposing effects in OA chondrocytes. Network pharmacology suggested that ART-related OA targets were enriched in inflammation-associated processes and signaling pathways (e.g., MAPK signaling), with PPI analysis highlighting inflammatory signaling hubs (e.g., JAK/STAT-related nodes). Consistently, molecular docking demonstrated favorable binding of ART within the MMP-13 active pocket, supporting the structural feasibility of an ART–MMP-13 interaction. Conclusion This study demonstrates that TGF-β1 plays an important pathogenic role in OA, as supported by MR and in vitro evidence, while ART exhibits anti-inflammatory and anti-catabolic effects by counteracting TGF-β1–driven inflammatory responses. Network pharmacology and docking analyses further suggest multi-target pathway regulation and a potential interaction with MMP-13. ART may represent a viable therapeutic candidate for OA; however, further studies are required to validate direct targets and elucidate tissue-specific mechanisms.
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高影响因子
Frontiers in Endocrinology
·
2022
·
IF 6.055
Nian Ding,Chenghong Zheng
By establishing a rat diabetes model in rats with intervening treatment by Jiangtang Tongmai Prescription (JTTMP), this study explored the restorative pairing effect of JTTMP on diabetic lung injury. The model of type II diabetes model was used to establish the rat diabetes model, using a high-fat diet and streptozotocin (STZ) induction. Different doses of JTTMP and metformin were administered as a therapeutic to intervene, and blood was collected to assess the blood glucose level of each group of rats. HE (Hematoxylin and eosin (H&E) staining was performed to detect the morphological changes in rat lung tissue and enzyme-linked immunoassay ELISA was used to detect and quantify the expression of interleukin (IL)-6, TNF tumor necrosis factor-ɑa, and IL-1β in serum and the lung tissue of each group of rats. The level expression of TGF-β1 [transforming growth factor (TGF)-β1), SnoN (transcriptional co-repressor Ski-N terminal (SnoN)], Smad2, Smad3, Smad7, and other signaling pathway proteins were assessed by Western blot. In comparison with the normal control (NC) group, rats in the diabetes model (DM) group lost weight and showed significantly increased blood sugar levels. The levels of TGF-β1 and Smad2/3 were increased in the DM group but Smad7 decreased. After 8 weeks of JTTMP intervention, the level of TGF-β1 and Smad2/3 decreased but Smad7 increased, blood sugar decreased significantly and the expression of inflammatory factors in lung tissue decreased. Therefore, JTTMP may activate SnoN and the downstream TGF-β1/Smads signaling pathway to repair diabetic lung injury, which suggests its application has potential for future clinical treatment of diabetes with lung injury.
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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病理学
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PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2026
·
IF 5.2
Qianqian Li,Yufang Ni,Zhaoyang Li,Yuanxia Zou,Huaiying Guo,Honglian Wang,Qiong Zhang,Li Wang,Jianchun Li
Chronic Kidney Disease (CKD) inevitably progresses to End-Stage Renal Disease (ESRD) via tubulointerstitial fibrosis, a process predominantly driven by the transforming growth factor-β (TGF-β)/SMAD family member 3 (Smad3) signaling pathway. Although curdione, a major sesquiterpenoid from Curcumae Rhizoma, exhibits anti-fibrotic activity, its specific mechanism in renal fibrosis remains undefined. Here, we investigated the protective effects of curdione using the Unilateral Ureteral Obstruction (UUO) mouse model and TGF-β1-stimulated renal tubular epithelial cells (TCMK1). We found that curdione (25 and 100 mg/kg) significantly mitigated UUO-induced renal injury and tubular necrosis, suppressed the injury marker kidney injury molecule-1 (KIM-1), and dose-dependently inhibited α-smooth muscle actin (α-SMA), fibronectin (FN), and Collagen I. Consistently, in TGF-β1-stimulated TCMK1 cells, curdione prevented fibrotic morphological changes and suppressed the upregulation of profibrotic markers. Mechanistically, curdione suppressed the expression of Filamin Binding LIM Protein 1 (Fblim1) and the phosphorylation of Smad2/3 in vivo and in vitro . Crucially, Fblim1 overexpression, achieved in vivo via ultrasound microbubble-mediated plasmid delivery and confirmed in vitro , significantly abrogated curdione’s anti-fibrotic effects and restored p-Smad3 levels. Furthermore, molecular docking predicted a strong binding affinity (-6.7 kcal/mol), while cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) assays physically validated that curdione directly binds to Fblim1, enhancing its molecular stability. In conclusion, this study provides convergent evidence at the tissue, cellular, and molecular levels that curdione exerts potent anti-fibrotic and renoprotective effects by directly targeting Fblim1, thereby functionally suppressing the TGF-β1/Smad3 signaling cascade. These findings establish curdione as a promising natural therapeutic candidate for CKD.
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高影响因子
PLoS Pathogens
·
2026
·Vol. 22
·期 5
·e1014007
·
IF 4.9
Xuejun Zhao,Xinyi Wang,Kejun Liu,Qian Fang,Cheng Wang,Guangbo Mei,Lihua Qu,Jiaxi Zhang,Jiayi Feng,Wenjuan Yang,Junnan Zhu,Hang Zhuo,Na Kuang,Xuebing Qiu,Zhigao Deng,Qiong Luo,Xiaoxia Jin,Lanxuan Jiang,Xiaoqing Li,Huifen Dong,Rui Zhou
Inhibiting the activation of hepatic stellate cells (HSCs) represents a key therapeutic strategy for alleviating liver fibrosis induced by schistosomiasis. Diverse cell populations secrete pro-inflammatory cytokines and chemokines, which induce HSC activation and thereby promote hepatic fibrosis progression. Tristetraprolin (TTP) exerts a pivotal role in the post-transcriptional regulation of pro-inflammatory cytokines by either accelerating mRNA degradation or suppressing translation, a regulatory mechanism closely associated with the pathogenesis of various hepatic disorders. However, the pathological roles of TTP in Schistosoma japonicum -induced liver fibrosis remain largely elusive. Here, we report that TTP is upregulated in the liver during S. japonicum -induced liver fibrosis, and its overexpression markedly ameliorates this fibrotic pathology in vivo . We further identify that TTP negatively regulates TGF-β1 mRNA stability by promoting N6-methyladenosine (m 6 A) RNA methylation, thereby inhibiting HSC activation. Mechanistically, TTP enhances transcription of the WT1-associated protein ( WTAP ) gene through its interaction with SMAD2/3. Furthermore, treatment with an m 6 A RNA methylation inhibitor confirms that TTP-mediated protection against S. japonicum -induced liver fibrosis, an effect associated with increased m⁶A RNA methylation in vivo . Thus, our findings uncover a novel and critical role of TTP in exerting its anti-fibrotic function via the WTAP/m 6 A epitranscriptomic machinery in the pathogenesis of S. japonicum -induced liver fibrosis. This finding provides a rationale for the therapeutic targeting of TTP-mediated m 6 A RNA methylation in S. japonicum -induced liver fibrosis.
Activation of hepatic stellate cells (HSCs) represents a pivotal event in the progression of schistosomiasis-induced liver fibrosis. Pro-inflammatory cytokines and chemokines secreted by injured hepatocytes and activated macrophage induce HSC activation. However, the underlying mechanisms governing the fine-tuned regulation of pro-inflammatory cytokines and chemokines gene expression during the progression of schistosomiasis-induced liver fibrosis remain largely elusive. As a key negative regulator of immune responses, the role of TTP in liver fibrosis remains controversial. Furthermore, while TTP has been reported to act as a transcriptional co-regulator and modulate gene expression at the transcriptional level, the majority of TTP-related studies have centered on its canonical role as a key mediator of mRNA degradation. Here, our study demonstrates that TTP attenuates S. japonicum -induced liver fibrosis via the regulation of TGF-β1 mRNA stability in an m 6 A-dependent manner. Specifically, WTAP-mediated m⁶A RNA methylation of TGF-β1 mRNA exerts a suppressive effect on HSC activation, thereby mitigating S. japonicum -induced liver fibrosis. Notably, our findings uncover a previously uncharacterized regulatory mechanism whereby TTP promotes WTAP transcription via direct interaction with SMAD2/3. These results demonstrate that TTP-driven transcriptional regulation of WTAP represents a novel mechanism underlying HSC activation, and further identify a potential strategy for intervening in S. japonicum -induced liver fibrosis.
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PubMed
高影响因子
TOXICOLOGY
·
2022
·
IF 4.571
Peng Lin,Xu Tong,Fan Xue,Chi Qianru,Tang Xinyu,Li Zhe,Bai Zhikun,Li Shu
Polystyrene nanoplastics (PS NPs) contamination is a serious problem for human and animal health. Excessive exposure to PS NPs can affect the structure and function of the heart. And lipopolysaccharide (LPS) induces myocardial damage , leading to myocardial fibrosis (MF). To investigate whether PS NPs exacerbate LPS-induced myocardial autophagy and fibrosis , we established in vivo and in vitro models of PS NPs/LPS exposure alone and in combination. We found that PS NPs/LPS exposure disrupts myocardial structure, significantly increases reactive oxygen species (ROS), triggers oxidative stress , promotes TGF-β1/Smad pathway activation, and leads to elevated levels of fibrotic proteins and collagen. Meanwhile, activation of AMPK/mTOR/ULK1 signaling pathway induced autophagy onset, and combined exposure of PS NPs/LPS exacerbated MF and autophagy. H9C2 cells were used for in vitro experiments, and the experimental results showed that the addition of TGF-β receptor inhibitor LY2109761 to the exposed group not only inhibited the upregulation of fibrotic genes but also effectively reduced the expression of autophagic signals, indicating that combined exposure of PS NPs and LPS mediates and regulates cardiac autophagy through TGF-β1. The above results suggest that PS NPs exacerbate LPS-induced MF and autophagy in mice via ROS/TGF-β1/Smad. Our study provides some new evidence to clarify the potential mechanisms of PS NPs-induced cardiotoxicity.
研究领域:
毒理学
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心脏病学
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纳米技术
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细胞生物学
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PubMed
高影响因子
AAPS PHARMSCITECH
·
2025
·Vol. 26
·期 5
·1-14
·
IF 4
Liu Hongting,Sun Yao,Cai Shihao,Zhao Conglu,xu Xiang,Xu Aiguo,Zhou Honggang,Yang Cheng,Gu Xiaoting,Ai Xiaoyu
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause, with few effective therapies available and high mortality rates. Our preceding research indicated that formononetin (FMN) could improve the symptoms of the bleomycin-induced pulmonary fibrosis and be a promising drug against IPF. In this study, an inhalable formononetin-loaded poly(lactic-co-glycolic) acid (PLGA) large porous microspheres (FMN-PLGA-MSs) was prepared by the method of emulsion solvent evaporation. SEM showed that FMN-PLGA-MSs were loose particles existing many pores on the surfaces, and the measured mean geometric diameter was more than 10 µm. The encapsulation efficiency (EE) and drug loading efficiency (DL) were 87.72 ± 6.34% and 4.18 ± 0.30%. FMN in FMN-PLGA-MSs could be rapidly released within 2 h and sustainably released for 21 d. Cell tests and q-RT-PCR tests showed that FMN could inhibit the activation of fibroblasts and the deposition of extracellular matrix (ECM) by acting on the TGF-β1/Smad3 signaling pathway. FMN-PLGA-MSs showed higher antifibrotic effects than free FMN oral administration in the pulmonary fibrosis models of mice, remarkably improving pulmonary function, decreasing hydroxyproline levels, and attenuating lung injuries. By formulating formononetin into microsphere preparations, its solubility can be significantly enhanced, enabling effective pulmonary drug delivery. This approach not only improves lung targeting but also reduces systemic toxicity. Additionally, it facilitates superior lung deposition and extends the retention time of the formononetin within the lungs. Taken together, FMN-PLGA-MSs may be a promising inhaled medication for the treatment of IPF. Graphical Formononetin (FMN) can improve the symptoms of idiopathic pulmonary fibrosis (IPF). Large porous microparticle can improve lung retention and lung targeting. FMN is loaded in poly(lactic-co-glycolic)acid (PLGA) to get microspheres (FMN-PLGA-MSs) for intratracheal instillation treatment of IPF. FMN-PLGA-MSs remarkably improved pulmonary function, decreased hydroxyproline, and attenuated lung injuries. FMN-PLGA-MSs are promising intratracheal instillation medication for the treatment of IPF.
研究领域:
药学
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呼吸病学
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分子生物学
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PubMed
高影响因子
RESPIRATORY RESEARCH
·
2025
·Vol. 26
·期 1
·1-15
·
IF 5
Wang Yudong,Liu Jun
Background Epithelial–mesenchymal transition (EMT) is regarded as a key process in repair of airway epithelium after injury. Forkhead Box C2 (FOXC2) is a transcription factor involved in EMT process, whether it is involved in repair of bronchial epithelium remains unknown.Methods C57BL/6 mice were subjected to intraperitoneal injection with naphthalene (NAPH; 200 mg/kg) to induce airway injury model. qPCR, immunoblot and FOXC2 immunohistochemistry assays were conducted to detect the expression of FOXC2 in bronchial epithelium. To explore the function of FOXC2 in NAPH-induced airway injury, the mice were given intratracheal administration of shFOXC2- or shNC-lentivirus particles, followed by NAPH treatment. Hematoxylin-and-eosin staining was used to assess the histopathology of the bronchial epithelium. Immunofluorescence analysis of CCSP, a club cell marker confirmed the CCSP expression in bronchial epithelium. Immunoblot and immunofluorescence assays determined the expression of E-cadherin, vimentin, and N-cadherin. In mouse primary bronchial epithelial cells (PBECs), we overexpressed and silenced FOXC2 by lentivirus particles, respectively. Cell migration was analyzed using wound healing assay. Immunoblot assays determined the E-cadherin, vimentin, FN-EDA expression in TGF-β1-induced PBECs. mRNA sequencing (mRNA-seq) and FOXC2 ChIP sequencing (ChIP-seq) to reveal the downstream genes of FOXC2 in TGF-β1-induced PBECs. Luciferase assay, ChIP-PCR and functional rescue experiments were performed to confirm the interaction of FOXC2/formin binding protein 1 (FNBP1) in TGF-β1-induced PBECs.Results FOXC2 expression was up-regulated in the lung tissues of mice at 2, 3 and 6 days post-NAPH. FOXC2 knockdown in bronchial epithelium of mice delayed CCSP+ club cell regeneration and normal repair of the airway epithelium within 14 days after injury. Knockdown of FOXC2 increased E-cadherin but decreased vimentin and N-cadherin, EMT markers during early phase after injury. In vitro, knockdown of endogenous FOXC2 repressed the migration of cells and increased TGF-β1-induced E-cadherin but decreased vimentin, N-cadherin and FN-EDA. Exogenous FOXC2 addition exerted opposite effects. Furthermore, mRNA-seq and FOXC2 ChIP-seq revealed that FNBP1 might be a downstream target of FOXC2. Overexpression of FNBP1 reversed the inhibitory role of FOXC2 knockdown in EMT.Conclusion sThese data highlight the important function of FOXC2 as a regulator in repair of bronchial epithelium after injury.Graphical
研究领域:
分子生物学
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呼吸系统疾病
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病理学
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PubMed
高影响因子
BMC CANCER
·
2022
·Vol. 22
·期 1
·1-12
·
IF 4.638
Chen Xueqin,Wang Yan,Liu Hancong,Zhang Jingjing,Wang Jie,Jin Xiaobao,Ma Yan
Background In our previous study, N end of the Circumsporozoite protein (CSP I-plus) modified recombinant human Endostatin (rEndostatin, endostar) (rES-CSP) was constructed, which had antiangiogenic capability and bound to hepatocellular carcinoma in vivo and in vitro. In this study, the inhibition of rES-CSP on hepatocellular carcinoma metastasis was verified in vivo and in vitro, and its possible mechanism was explored. Methods Firstly, the impact of rES-CSP on the migration, adhesion of hepatoma cell HCCLM3 was identified by wound healing, transwell, and on metastasis of orthotopic xenograft model was identified in nude mouse. Then the expression of metastasis-associated molecules (MMP2, E-cadherin, integrinβ1) and angiogenesis-related factors (VEGFA) in vitro and in vivo were detected by real-time PCR, western blotting, immunohistochemistry. Results Finally, we found that rES-CSP could inhibit the migration and invasion of HCCLM3, and decrease tumor metastasis and growth in nude mouse orthotopic xenograft models. The tumor inhibiting rates of rES-CSP and Endostar were 42.46 ± 5.39% and 11.1 ± 1.88%. The lung metastasis rates of the control, Endostar and rES-CSP were 71, 50, and 42.8%, respectively. Compared with Endostar, rES-CSP significantly down-regulated the expression of VEGFA and integrinβ1. Heparin, a competitive inhibitor of CSP I-plus, which can be bind to the highly-sulfated heparan sulfate proteoglycans (HSPGs) over-expressed in liver and hepatocellular carcinoma, alleviated the down-regulation of VEGFA and integrinβ1. Conclusions These indicate that rES-CSP may play a role in inhibiting tumor growth and metastasis by down-regulating the angiogenic factor VEGF and the metastasis-related molecules or by interfering with HSPGs-mediated tumor metastasis.
研究领域:
肿瘤学
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分子生物学
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药理学
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PubMed
高影响因子
Journal of Materials Chemistry B
·
2019
·Vol. 7
·期 42
·6604-6611
·
IF 5.047
Ying Xie,Hua Wang,Jinzhu Mao,Yuce Li,Mubashir Hussain,Jinjin Zhu,Yan Li,Lianbin Zhang,Juan Tao,Jintao Zhu
Hypertrophic scarring is a widespread skin disorder that affects a patient's confidence and quality of life. Intralesional injection of bleomycin is one of the most commonly employed treatments for hypertrophic scars, which, however, always brings pain and requires long-term treatment. To overcome these limitations, new methods for bleomycin delivery enabling painlessness, self-administration, the fast onset of action, and good bioavailability are urgently needed. In this study, we developed bleomycin-loaded dissolving microneedles (BMN) made up of hyaluronic acid (HA) with excellent aqueous solubility and enhanced efficacy for inhibiting hypertrophic scars. The as-obtained BMN possesses sufficient mechanical strength to pierce porcine skin ex vivo with an insertion depth of over 300 μm. Moreover, BMN can dissolve rapidly and release 20% of loaded bleomycin within 1 min and 52% within 10 min, and the BMN-treated skin could recover to its original status within 3 h, demonstrating good biocompatibility. Besides, the HA matrix also maintains the stability and activity of bleomycin. Furthermore, we show that BMN consisting of HA and bleomycin can inhibit the proliferation of human hypertrophic scar fibroblasts (hHSFs) and the secretion of transforming growth factor-β (TGF-β1) in vitro. Therefore, bleomycin-loaded dissolving HA microneedles provide a potential route to treat hypertrophic scars in a convenient, efficient, and minimally invasive manner.
研究领域:
皮肤科
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药剂学
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生物医学工程
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伤口愈合
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PubMed
高影响因子
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