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
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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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PubMed
高影响因子
Cells
·
2026
·Vol. 15
·期 19
·1765
·
IF 6
Lin Guo 1,2,†,Yuanli He 1,†,Feiming Hu 1,†,Yuanjie Sun 1,†,Yajie Zhang 1,3,Junyi Ren 4,Ren Zheng 1,Junqi Zhang 1,Yubo Sun 1,Sirui Cai 1,Yueyue Wang 1,Kun Yang 1,Chenchen Hu 1,* andShuya Yang
Cervical cancer remains one of the major gynecological malignancies worldwide, with tumor immune evasion playing a critical role in disease progression. Although accumulating evidence has implicated BAP31 in tumor progression and immune regulation, its role in immune evasion in cervical cancer remains poorly understood. In this study, we found that BAP31 was significantly upregulated in cervical cancer tissues and that elevated BAP31 expression was associated with poor patient prognosis. Functional assays demonstrated that BAP31 silencing restored the immune activity of dendritic cells. Mechanistically, BAP31 was found to regulate TGF-β at the post-transcriptional level and to facilitate its transport from the endoplasmic reticulum to the Golgi apparatus through an interaction involving the Asn-381 residue, thereby affecting its intracellular maturation and extracellular secretion. Additional functional analyses showed that exogenous TGF-β impaired dendritic cell maturation and migration while enhancing phagocytic activity. Collectively, these findings indicate that BAP31 regulation of TGF-β contributes to dendritic cell dysfunction and the establishment of an immunosuppressive microenvironment in cervical cancer.
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高影响因子
Frontiers in Medicine
·
2026
·
IF 3.6
Wenbing Lai,Lurun Wang,Wei Tang,Yuze Liu
Background Skin photoaging, primarily caused by chronic ultraviolet B (UVB) exposure, is characterized by cellular senescence and extracellular matrix (ECM) degradation. Suppression of transforming growth factor-β (TGF-β)/Smad signaling plays a critical role in UVB-induced collagen loss and impaired skin repair. Azelaic acid (AzA), a clinically established dermatological agent with antioxidant and anti-inflammatory properties, has been reported to maintain skin homeostasis; however, its mechanistic role in protecting against UVB-induced photoaging remains unclear. Objective This study aimed to investigate whether AzA alleviates UVB-induced photoaging in keratinocytes and to determine whether its protective effects are mediated through the restoration of Smad-dependent TGF-β signaling. Methods An in vitro UVB-induced photoaging model was established using HaCaT keratinocytes. Following UVB irradiation, cells were treated with AzA. Cell viability and cytotoxicity were evaluated using CCK-8 and LDH assays, respectively. Cellular senescence was assessed by senescence-associated β-galactosidase staining. ECM-related markers were measured by ELISA. TGF-β/Smad signaling activity was analyzed by Western blotting, quantitative real-time PCR, and immunofluorescence. The selective TGF-β/Smad inhibitor SB431542 was used to verify pathway dependence. A keratinocyte–fibroblast conditioned medium model was also employed to assess the paracrine regulation of fibroblast ECM metabolism. Results AzA significantly attenuated UVB-induced cellular senescence and partially restored cell viability in HaCaT cells. It significantly increased pro-collagen I levels and reduced MMP-1 levels, indicating the restoration of ECM-related protein balance. Mechanistically, AzA reversed UVB-induced suppression of TGF-β/Smad signaling by enhancing Smad2/3 phosphorylation, decreasing Smad7 expression, promoting the nuclear translocation of phosphorylated Smad2/3, and restoring Smad-dependent transcription. Pharmacological inhibition of TGF-β/Smad signaling largely abrogated these protective effects. Conditioned medium from AzA-treated keratinocytes also improved ECM-related responses in fibroblasts in a Smad-dependent manner. Conclusion AzA alleviates UVB-induced photoaging by restoring Smad-dependent TGF-β signaling, preserving ECM homeostasis, and modulating epidermal–dermal crosstalk in vitro. These findings provide mechanistic support for the potential application of AzA in anti-photoaging strategies.
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PubMed
高影响因子
POLYMER TESTING
·
2026
·
IF 6.4
Wei Zhan,Hui Deng,Yifeng Xia,Xiao Liu,Jinping You,Fanrong Ai,Jinjun Huang
Microspheres can efficiently load and sustainably deliver growth factors and stem cells. • Microspheres provide a favorable microenvironment that supports chondrogenic differentiation of stem cells. • Injectable microspheres can be applied to irregular and complex cartilage defects in a minimally invasive manner. • Microspheres loaded with stem cells and growth factors offer a new strategy for cartilage defect repair. Cartilage defects severely compromise patients’ quality of life, as the unique structural characteristics of native cartilage endow it with extremely limited self-repair capacity. Mesenchymal stem cells (MSCs) possess tremendous therapeutic potential for cartilage tissue engineering due to their multilineage differentiation capability; however, technical bottlenecks associated with current cell delivery systems greatly restrict their clinical translation. Herein, we fabricated an injectable, multifunctional hydrogel microsphere system (PGCT-MS). Specifically, arginine-glycine-aspartate (RGD) sequences conjugated on gelatin molecules facilitate MSC adhesion, while chondroitin sulfate—an essential component of the chondrocyte extracellular matrix—constructs a favorable microenvironment for MSC spreading. Moreover, polydopamine modification on the microsphere surface enables efficient immobilization and sustained release of transforming growth factor-β3 (TGF-β3), which effectively induces the chondrogenic differentiation of bone marrow MSCs (BMSCs) at cartilage defect sites after in situ injection. In vitro experimental results demonstrated that PGCT-MS significantly enhances BMSC adhesion and chondrogenic differentiation, as verified by the upregulated expression of chondrogenic marker genes, and exhibits excellent adhesion affinity for native cartilage matrices. In vivo animal studies further validated that BMSC-loaded PGCT-MS markedly accelerates high-quality cartilage regeneration. Collectively, this multifunctional therapeutic delivery system provides a promising and feasible strategy for clinical cartilage defect repair.
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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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DOI
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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DOI
PubMed
高影响因子
Chemical Biology & Drug Design
·
2025
·Vol. 106
·期 6
·e70226
·
IF 3.3
Yaqiong Wang,Li Ma
Pachymic acid exerts antitumor effects against renal cell carcinoma and breast, lung, and pancreatic cancers; however, its specific inhibitory effect on endometrial cancer progression remains unclear. Therefore, in this study, we investigated the antitumor effects of pachymic acid against endometrial cancer using cell counting kit 8, flow cytometry, wound healing, transwell, cycloheximide chase, and western blot assays. Notably, pachymic acid significantly suppressed the viability, proliferation, and migration of endometrial cancer cells. Nuclear receptor subfamily 3 group C member 1 (NR3C1) was identified as its potential target against endometrial cancer. Pachymic acid promoted NR3C1 degradation. However, NR3C1 overexpression reversed the inhibitory effects of pachymic acid on the proliferation and migration of endometrial cancer cells. Furthermore, an association was observed between NR3C1 expression and the transforming growth factor beta (TGF-β) pathway. NR3C1 knockdown and pachymic acid treatment reduced protein levels of TGF-β1 and p-Smad2/3. TGF-β pathway inhibitor galunisertib reversed the NR3C1 overexpression-induced increase in endometrial cancer cell migration. Collectively, our findings suggest that pachymic acid suppresses endometrial cancer cell migration by inhibiting the NR3C1/TGF-β/Smad signaling pathway, highlighting its potential as a therapeutic agent for endometrial cancer.
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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细胞生物学
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天然产物研究
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
·
2026
·
IF 1.9
Zhiyi Zhang,Haipeng Yu,Liqun Hao
As a key component of the replication protein A (RPA) complex, RPA3 has been identified as oncogenic in multiple solid tumors. However, its specific role in breast cancer remains poorly understood. RPA3 expression and its prognostic relevance in breast cancer were assessed based on the public databases. To further confirm the biological function of RPA3, we knocked down RPA3 in the breast cancer cell line Michigan Cancer Foundation-7 (MCF-7) and then conducted Cell Counting Kit-8, colony formation, Western blot, immunofluorescence, and transmission electron microscopy. In vivo effects of RPA3 were tested in a xenograft model. We found that high expression of RPA3 in breast cancer predicted adverse patient outcomes. RPA3 was mainly involved in multiple oncogenic signaling pathways, including the transforming growth factor-β (TGF-β) pathway. RPA3 knockdown effectively suppressed cancer cell proliferation in vitro and in vivo. Mechanistically, RPA3 knockdown decreased TGF-β1 promoter activity and reduced TGF-β1 expression at mRNA and protein levels, accompanied by decreased p-Smad2/3 levels. RPA3 knockdown also significantly blocked autophagy, as evidenced by decreased microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I ratio, increased sequestosome 1 (p62) level, and reduced LC3 puncta. Notably, pharmacological activation of the TGF-β pathway partially reversed autophagy alterations induced by RPA3 knockdown. These data support the possibility of RPA3 as a therapeutic target for breast cancer.
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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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高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2025
·
IF 2.2
Meng Zhang,Congyao Wang,Ruiqi Zhao,Jiabo Yuan
Background Asthma is a chronic disease characterized by airway remodeling, which results in a progressive decline in lung function. Senkyunolide A is one of the effective components of ligusticum chuanxiong Hort, it shows protective effects on many human diseases. However, the role of Senkyunolide A in asthma remains unclear. Results In our study, we established an asthma mouse model by ovalbumin (OVA) sensitization and challenge, and Senkyunolide A (20 mg/kg and 40 mg/kg) was given by intraperitoneal injection. For in vitro study, lung epithelial BEAS-2B cells were treated with TGF-β1 to induce epithelial mesenchymal transformation. Our study showed that Senkyunolide A (40 mg/kg) alleviated airway injury, inflammatory infiltration and airway remodeling induced by OVA in asthma mice. Meanwhile, Senkyunolide A (40 μM) recovered the high level of cell migration and profibrotic factors expression induced by TGF-β1. Mechanistically, Senkyunolide A abolished the effect of OVA or TGF-β1 on Smad2/3 phosphorylation at site Ser 465/467 /Ser 423/425 in mice or BEAS-2B cells and inhibited the activation of NLRP3 inflammasome induced by OVA. Conclusions In total, our study indicated that Senkyunolide A alleviated airway damage and airway remodeling in asthmatic mice and regulated the progress of asthma by inhibiting the TGF-β/Smad2/3 signaling pathway and NLRP3 activation.
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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
·
细胞生物学
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DOI
PubMed
高影响因子
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