Latest ArticlesLiver fibrosis is a common pathological process that many chronic liver diseases must undergo to develop into cirrhosis and hepatocellular carcinoma. Liver fibrosis is regulated by a variety of cytokines and signal pathways during its occurrence and development. In recent years, a large number of studies showed that ferroptosis is closely related to liver fibrosis. Compared with normal liver, the levels of irons and lipid peroxidation in the liver with fibrosis are significantly increased. Therefore, ferroptosis may be a potential target for the diagnosis, prevention, and treatment of liver fibrosis. This review summarizes the role of ferroptosis in liver fibrosis, thus to provide new ideas for the treatment of liver fibrosis.
Idiopathic pulmonary fibrosis is a fibrous disease. At present, its pathogenesis has not been fully elucidated and there is no drug with definite therapeutic effect. After four stages of development, antibody drugs are becoming a new hotspot in drug research and development with their own advantages. A number of drugs have entered the stage of clinical trials. Based on this, this review summarizes the antibody drugs for the clinical stage of clinical research of idiopathic pulmonary fibrosis, in order to summarize the development of antibody drugs, and provide certain bases and ideas for the development of antibody drugs.
Idiopathic pulmonary fibrosis (IPF) is an irreversible and highly mortal interstitial disease. The incidence of IPF is increasing around the world, which seriously harms human health and brings huge economic burden to the society. While traditional treatments can slow the progression of the disease, they are far to cure this disease. Clinically, pirfenidone and nintedanib are two main drugs that used for the treatment of IPF. However, severe adverse reactions were reported in some patients. Therefore, it is very important to explore novel therapeutic strategies to reverse fibrosis and regenerate lung. The repair and regeneration ability of stem cells has unique advantages in the treatment of pulmonary fibrosis. The structure and function of organoids produced by stem cells have similar characteristics with live organs. Therefore, lung stem cells play an important role in the discovery of novel anti-IPF drugs, and in the formation and development of lung tissue. In addition, organoids produced by stem cells also serve as a perfect model for regenerative medicine. In this review, we mainly summarize the role of stem cells and organoids in the repair and regeneration of pulmonary fibrosis, and hope to provide a reference for the development of clinical treatment of pulmonary fibrosis.
Epithelial mesenchymal transition (EMT) is a reprogramming process of epithelial to mesenchymal transition, in which epithelial cells lose polarity and intercellular adhesion and acquire stronger migration and invasion ability similar to mesenchymal cells. EMT is a critical step during the pathogenesis of pulmonary fibrosis. Lung epithelial cells can differentiate into myofibroblasts through EMT, which accelerates the fibrosis process. In recent years, a large number of studies have shown that non-coding RNAs (ncRNAs) are involved in the EMT process of lung epithelial cells, at the same time, some natural medicines were found to prevent and treat pulmonary fibrosis by intervening in ncRNAs related to pulmonary fibrosis. In this review, we summarize the expression change and biological function of vital ncRNAs in EMT progression during pulmonary fibrosis, as well as the research progress of EMT related ncRNA mediated by natural medicines on pulmonary fibrosis, aiming to provide new insights into the research of ncRNAs and the exploration of new pharmacological targets of natural medicine.
S-phase kinase-associated protein 2 (Skp2) is one of the components of E3 ubiquitin ligase, which can induce proteasome-mediated proteolysis or regulate labeled substrates to promote cell proliferation and migration and inhibit cell apoptosis and senescence by connecting the ubiquitin chains of K48 and K63 to different substrates. Skp2 is also a potential drug target in a variety of fibrotic diseases, is highly expressed in a variety of fibrotic diseases, and regulates the occurrence and progression of these diseases. This paper reviews Skp2's structure, downstream targets, and cellular regulation and then focuses on research progress on Skp2 in various fibrotic diseases, such as liver fibrosis, idiopathic pulmonary fibrosis, renal fibrosis, corneal fibrosis, and cardiac fibrosis, which may help provide a new research approaches for clinical development of Skp2-targeted antifibrotic drugs.
Cardiac fibrosis is a vital pathological feature of various cardiovascular diseases, including myocardial infarction and heart failure. However, there have been few clinical interventions to treat cardiac fibrosis. Noncoding RNAs (ncRNAs) are a class of RNAs that do not encode proteins. ncRNAs participate in various cellular biological processes and regulate gene expression at transcription, post-transcription and epigenetic levels. Recent studies demonstrate that ncRNAs participate in the regulation of cardiac fibrosis by affecting the proliferation and transition of cardiac fibroblasts. ncRNAs can be used as potential intervention targets and biomarkers for cardiac fibrosis, provide new strategies and approach for treating and preventing fibrosis associated cardiovascular diseases. This review summarizes the function and mechanisms of ncRNAs in cardiac fibrosis.
We aimed to explore the involvement of Fas-associated death domain protein (FADD) in the inhibitory effects of etoposide (VP16) on the proliferation, migration, and apoptosis of A549 non-small cell lung cancer (NSCLC) cells. FADD knockout (KO) and control A549 cells were constructed using the CRISPR/Cas9 system. The cell counting kit-8 (CCK-8) assay, the scratch wounding assay, and the Annexin V/PI staining-based flow cytometry were used to assess the effect of FADD KO on viability, migration, and apoptosis of A549 cells with or without the presence of etoposide, respectively. The expression pattern of several proteins involved in proliferation[raf proto-oncogene serine/threonine-protein kinase (c-Raf) and extracellular signal-regulated kinase of phosphorylation (p-ERK)], apoptosis[B-cell lymphoma 2 (BCL2), cleaved cysteinyl aspartate specific proteinase 3 (cleaved-caspase-3), and cleaved-caspase-9] and migration[matrix metalloproteinase 2 (MMP2)] was detected by Western blot. We found that FADD KO attenuated proliferation and migration of A549 cells. Consistently, we demonstrated that FADD KO enhanced etoposide-mediated inhibition of proliferation and migration in A549 cells. We further demonstrated that FADD KO obviously enhanced etoposide-mediated apoptosis in A549 cells. For mechanism exploration, we found that etoposide sensitivity enhanced by FADD KO may be partly explained by reduced expression of c-Raf, p-ERK, MMP2, and increased cleavage of caspase-3 and -9. Combined with the Kaplan-Meier (KM) survival curve analysis obtained from the GEPIA database, it is preliminarily judged that patients with high FADD gene levels in lung adenocarcinoma have a poor prognosis. Our study suggests that FADD can be used as a potential biomarker for the treatment of lung adenocarcinoma, providing a personalized treatment plan for the treatment of lung adenocarcinoma.
The movement and deposition of inhaled particles in the lung tissue have an important influence on the respiratory physiology of human body. The corresponding particle dynamics model plays a vital role in exploring the pathogenic factors and treatment methods of lung diseases. Such as evaluating the optimal design of pulmonary atomization drug delivery and the impact of particulate air pollutants on the lung. According to the different knowledge and modeling methods, this paper classifies, combs and analyzes several representative particle dynamics models in lung airways in recent years. We divided the mechanism models into the biological model, physical model and numerical simulation model. The biological models include in vivo imaging and pharmacokinetic methods; physical models include bionic and microfluidic chip models; the numerical models include respiratory tract model, airflow model and particle model. Moreover, the numerical solution and fluid-structure-interaction models were also reviewed, especially the application prospect of the lattice Boltzmann method.
Conjugated linoleic acid (CLA) is a nutrient substance that exists in humans and animals. It has anti-tumor, anti-atherosclerosis, and immune-regulating functions, but its oral bioavailability is low. Conjugated linoleic acid dry powder inhalers (CDPIs) were prepared and intratracheally administered to the rats that suffered from primary lung cancer. Conjugated linoleic acid nanoemulsions were prepared first and CDPIs were with 10% mannitol after lyophilization. CDPIs are loose white powders with the aerodynamic median diameter (Da) of 3.10 μm, which were suitable for pulmonary delivery. Rats lung cancer models were established after 45 days by instilling 3-methylcholanthrene (MCA) and N, N-dimethylnitrosamine (DEN) into the rats lung once. The animal experiments were approved by the Ethics Committee of Academy of Military Medical Sciences and conducted in accordance with the relevant guidelines and regulations. The CDPIs, gefitinib suspension and blank DPIs were sprayed into the lungs of rats with lung cancer through the trachea. Compared with the model group, both the gefitinib suspension group and the CDPIs group showed significantly fewer tumor nodules and inflammatory cells, and the CDPIs group was better than the gefitinib suspension group. The inhibition efficiency of CDPIs on CD31 and NF-κB p65 was better than that of the gefitinib suspension group. The vascular endothelial growth factor (VEGF) level in the CDPIs group was significantly reduced, which was equivalent to that of the gefitinib suspension group. The apoptosis in the CDPIs group by Tunel tests showed a significant increase, which was significantly better than the gefitinib suspension group. Therefore, CDPIs had excellent pharmacological activity on lung cancer, which provided a model for the efficient delivery of oil therapeutic agents.
Transient receptor potential vanilloid ion channel subtypes 2 (TRPV2) is a calcium permeable nonselective cation channel. TRPV2 is expressed in nerves, blood vessels, spleen, and other organs, and participates in the regulation of a variety of important physiological functions, such as nociception, neural development, and immune response. Here we reviewed the research progress on the structure, modulators, and physiological functions of TRPV2 channel to provide references for future research.
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