Chlorogenic acid attenuates idiopathic pulmonary fibrosis: An integrated analysis of network pharmacology, molecular docking, and experimental validation.

Aims: Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung condition, the cause of which remains unknown and for which no effective therapeutic treatment is currently available. Chlorogenic acid (CGA), a natural polyphenolic compound found in different plants and foods, has emerged as a promising agent due to its anti-inflammatory, antioxidant, and antifibrotic properties. However, the molecular mechanisms underlying the therapeutic effect of CGA in IPF remain unclear.

Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible disease with a high mortality rate worldwide. However, the etiology and pathogenesis of IPF have not yet been fully described. Moreover, lung cancer is a significant complication of IPF and is associated with increased mortality.

-Derived Extracellular Vesicles Attenuate Bleomycin-Induced Pulmonary Fibrosis Trough Antioxidant, Anti-Inflammatory and Protease Activity in a Mouse Model.

Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe idiopathic interstitial pneumonia. It is a chronic and progressive disease with a poor prognosis and is a major cause of morbidity and mortality. This disease has no cure; therefore, there is a clinical need to search for alternative treatments with greater efficacy.

Coadministration of 3'5-dimaleamylbenzoic acid and quercetin decrease pulmonary fibrosis in a systemic sclerosis model.

Systemic sclerosis (SSc) is an autoimmune disease characterized by microvascular compromise and fibrosis. Pulmonary fibrosis, a prominent pulmonary complication in SSc, results in impaired lung function due to excessive accumulation of extracellular matrix components. This study aimed to investigate the effects of coadministration of 3'5-dimaleamylbenzoic acid (AD) and quercetin (Q) on key events in the development and maintenance of pulmonary fibrosis in a bleomycin (BLM)-induced SSc mouse model.

Evaluation of renal damage in a bleomycin-induced murine model of systemic sclerosis.

Objectives: Systemic sclerosis (SSc) is an autoimmune disease of unknown etiology with a high mortality rate. Renal crisis has been reported as one of the predictors of early mortality in these patients. The present study was performed to evaluate bleomycin-induced SSc using an osmotic minipump as a possible model for the analysis of renal damage in SSc.

miRNAs Contained in Extracellular Vesicles Cargo Contribute to the Progression of Idiopathic Pulmonary Fibrosis: An In Vitro Aproach.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease. Lesions in the lung epithelium cause alterations in the microenvironment that promote fibroblast accumulation. Extracellular vesicles (EVs) transport proteins, lipids, and nucleic acids, such as microRNAs (miRNAs).

Quercetin Regulates Key Components of the Cellular Microenvironment during Early Hepatocarcinogenesis.

Hepatocellular carcinoma (HCC) is a health problem worldwide due to its high mortality rate, and the tumor microenvironment (TME) plays a key role in the HCC progression. The current ineffective therapies to fight the disease still warrant the development of preventive strategies. Quercetin has been shown to have different antitumor activities; however, its effect on TME components in preneoplastic lesions has not been fully investigated yet.

The Role of Extracellular Vesicles in Idiopathic Pulmonary Fibrosis Progression: An Approach on Their Therapeutics Potential.

Idiopathic pulmonary fibrosis (IPF) is a fibrosing interstitial lung disease of unknown etiology. Different types of cells are involved in fibrogenesis, which is persistently physical and molecular stimulation, either directly or by interacting with bioactive molecules and extracellular vesicles (EVs). Current evidence suggests that EVs play an essential role in IPF development.

The implications of ABCC3 in cancer drug resistance: can we use it as a therapeutic target?

Drug resistance is one of the main causes of chemotherapy failure. Although several factors are involved in cancer drug resistant, the exporter pumps overexpression that mediates the drugs flow to outside the cells and reduces both the drugs intracellular concentration and effectiveness, has been one of the most important challenges. Overexpression of ABCC3, a member of the ABCC subfamily, has been strongly associated to the resistance to multiple drugs.

Involvement of 4-hydroxy-2-nonenal in the pathogenesis of pulmonary fibrosis.

Pulmonary fibrosis is a chronic progressive disease with high incidence, prevalence, and mortality rates worldwide. It is characterized by excessive accumulation of extracellular matrix in the lung parenchyma. The cellular and molecular mechanisms involved in its pathogenesis are complex, and some are still unknown.

Proteomic Analysis Reveals Key Proteins in Extracellular Vesicles Cargo Associated with Idiopathic Pulmonary Fibrosis In Vitro.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, and highly fatal disease. It is characterized by the increased activation of both fibroblast and myofibroblast that results in excessive extracellular matrix (ECM) deposition. Extracellular vesicles (EVs) have been described as key mediators of intercellular communication in various pathologies.

Liver damage in bleomycin-induced pulmonary fibrosis in mice.

Pulmonary fibrosis is an emerging disease with a poor prognosis and high mortality rate that is even surpassing some types of cancer. This disease has been linked to the concomitant appearance of liver cirrhosis. Bleomycin-induced pulmonary fibrosis is a widely used mouse model that mimics the histopathological and biochemical features of human systemic sclerosis, an autoimmune disease that is associated with inflammation and expressed in several corporal systems as fibrosis or other alterations.