A5061373655- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pulmonary Hypertension Research and Treatments
- Peptidase Inhibition and Analysis
- Neonatal Respiratory Health Research
- Eosinophilic Disorders and Syndromes
- Pleural and Pulmonary Diseases
- Lung Cancer Treatments and Mutations
- Medical Imaging and Pathology Studies
- Pneumocystis jirovecii pneumonia detection and treatment
- Occupational exposure and asthma
- Quinazolinone synthesis and applications
- Phagocytosis and Immune Regulation
- Silymarin and Mushroom Poisoning
- Wnt/β-catenin signaling in development and cancer
- Polyomavirus and related diseases
- Chemical Reactions and Isotopes
- Inhalation and Respiratory Drug Delivery
- Heat shock proteins research
- Extracellular vesicles in disease
- Cardiac Structural Anomalies and Repair
- Educational Management and Quality
- Plant Toxicity and Pharmacological Properties
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Multiple Myeloma Research and Treatments
- Eosinophilic Esophagitis
State Key Laboratory of Medicinal Chemical Biology
2018-2024
Nankai University
2017-2024
Tianjin International Joint Academy of Biomedicine
2019-2020
Tianjin University
2019
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease, and the molecular mechanisms remain poorly understood. Our findings demonstrated that pyruvate kinase M2 (PKM2) promoted progression by directly interacting with Smad7 reinforcing transforming growth factor-β1 (TGF-β1) signaling. Total PKM2 expression portion of tetrameric form elevated in lungs fibroblasts were derived from mice bleomycin (BLM)-induced fibrosis. Pkm2 deletion markedly alleviated BLM-induced...
Abstract Objectives Anlotinib hydrochloride (AL3818) is a novel multitarget tyrosine kinase inhibitor which has the same targets as nintedanib, an effective drug been approved for treatment of idiopathic pulmonary fibrosis. Here, we examined whether anlotinib could also attenuate bleomycin-induced fibrosis in mice and explored antifibrosis mechanism. Methods We have evaluated effect on mice. Inflammatory cytokines alveolar lavage fluid including IL-1β, IL-4, IL-6 TNF-α were determined by...
Idiopathic pulmonary fibrosis (IPF) is a progressive and usually fatal lung disease that characterized by fibroblast proliferation extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture formation focal fibrous hyperplasia. The molecular mechanism develops not fully understood, no satisfactory treatment currently exists. However, many studies consider aberrant activation TGF-β1 frequently promotes epithelial-mesenchymal transition (EMT) fibrosis....
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease of unknown cause and characterized by excessive proliferation fibroblasts the irregular remodeling extracellular matrix (ECM), which ultimately severe distortion alveolar architecture. The median survival IPF patients 2-5 years. are predominantly infiltrated M2 macrophages during course development progression. Predominantly accumulation accelerates progression secreting multiple cytokines that promote fibroblast to...
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease with multiple causes, characterized by excessive myofibrocyte aggregation and extracellular matrix deposition. Related studies have shown that transforming growth factor-β1 (TGF-β1) key cytokine causing fibrosis, promoting abnormal epithelial-mesenchymal communication fibroblast-to-myofibroblast transition. Fedratinib (Fed) marketed drug for the treatment of primary secondary myelofibrosis, targeting...
Idiopathic pulmonary fibrosis (IPF) is one of the most fatal chronic interstitial lung diseases with unknown pathogenesis, current treatments cannot truly reverse progression disease. Pulmonary macrophages, especially bone marrow derived pro-fibrotic secrete multiple kinds profibrotic mediators (SPP1, CD206, CD163, IL-10, CCL18…), thus further promote myofibroblast activation and procession. IL20Rb a cell-surface receptor that belongs to IL-20 family. The role in macrophage remains unclear....
Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by epithelial cell damage, myofibroblast activation, and collagen deposition. Multiple studies have documented that the Wnt/β-catenin pathway aberrantly activated in IPF plays a vital role differentiation activation. Kinases such as Src initiate signaling phosphorylating β-catenin at tyrosine residues, which facilitates accumulation nucleus promotion of progression. Nintedanib has been approved for treatment...
Idiopathic pulmonary fibrosis (IPF) is a progressive, life-threatening lung disease characterized by the proliferation of myofibroblasts and deposition extracellular matrix that results in irreversible distortion structure formation focal fibrosis. The molecular mechanism IPF not fully understood, there no satisfactory treatment. However, most studies suggest abnormal activation transforming growth factor-β1 (TGF-β1) can promote fibroblast epithelial to mesenchymal transition (EMT) induce...
Sesquiterpene lactones (SL) have a wide range of applications in anti-tumor and anti-inflammatory therapy. However, the pharmacological mechanism such substances is not clear. In this study, parthenolide (PTL) was used as an example to explore effect natural molecules their common mechanism. We showed that PTL inhibited proliferation migration by reverse EMT via ERK2/NF-κB/Snail pathway vivo vitro. Interestingly, Multiple potential targets contain Gly-Leu-Ser/Lys-"co-adaptation pocket". This...
Idiopathic pulmonary fibrosis (IPF) is a heterogeneous group of lung diseases with different etiologies and characterized by progressive fibrosis. This disease usually causes structural remodeling decreased function. The median survival IPF patients 2–5 years. Predominantly accumulation type II innate immune cells accelerates progression secreting multiple pro-fibrotic cytokines. Group 2 lymphoid (ILC2) monocytes/macrophages play key roles in immunity aggravate the formation environment. As...
<b>Background:</b> Idiopathic pulmonary fibrosis is incurable and has no effective treatment. The marketed drugs are only pirfenidone nintedanib. By evaluating the inhibition effects of nintedanib on proliferation, migration activation human lung fibroblasts (HFL1), anti-fibrotic mechanism two was tested compared to provide reference for accurate clinical medication. <b>Methods:</b> HFL1 cells were divided into control group, TGF-β1/ PDGF-stimulate-model drug-add group. effect proliferation...
<b>Background:</b> Pirfenidone(PFD) and nintedanib(NDN), the only two drugs for IPF, which should be accurately selected in treatment, has no relevant basic research reference. <b>Objective:</b> Compare effect of PFD NDN bleomycin(BLM)-induced pulmonary fibrosis model different periods, so as to provide theoretical basis clinical application. <b>Methods:</b> The BLM periods were performed Fig1. <b>Results:</b> 1) Anti-inflammatory antioxidant capacity: inhibition rate on inflammatory cell...
Pulmonary fibrosis is a pathological consequence of interstitial pulmonary diseases, and characterized by the persistence fibroblasts excessive deposition extracellular matrix. The etiology multifactorial, role inflammation as an important component in IPF controversial sometimes seen epiphenomenon fibrosis. Stimulus increase production pro-inflammatory cytokines activation NF-κB, which will further promote response myofibroblast transition. Lenalidomide immunomodulatory drug. Previous study...