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Remodelación de las vías respiratorias: mecanismos clave y conocimientos clínicos
- 2025
- 2024
- 2023
Autores: Zhang B, Feng X, Tian L, et al.
Publicación: 22 Enero 2025
Transición epitelio-mesenquimal en el asma: su papel y mecanismos reguladores subyacentes
Abstract
Bronchial asthma (asthma) is a respiratory disease characterized by chronic inflammation, airway hyperresponsiveness, and airway remodeling. Numerous studies have delved into asthma's pathogenesis, among which epithelial mesenchymal transition (EMT) is considered one of the important mechanisms in the pathogenesis of asthma. EMT refers to the transformation of epithelial cells, which lose their original features and acquire a migratory and invasive stromal phenotype. EMT contributes to normal physiological functions like growth, development, and wound healing. However, EMT is also involved in the occurrence and development of many diseases. Currently, the precise regulatory mechanism linking EMT and asthma remain obscure. Increasing evidence suggests that airway EMT contributes to asthma pathogenesis via dysregulation of associated control mechanisms. This review explores EMT's significance in asthma and the regulatory networks associated with EMT in this context.
ES-41206 Marzo 2026
Autores: Lim EY, Kim GD.
Publicación: 17 Octubre 2024
Efectos emergentes sobre la salud inducidos por las partículas asociadas con el estrés oxidativo y la inflamación
Abstract
Environmental pollution continues to increase with industrial development and has become a threat to human health. Atmospheric particulate matter (PM) was designated as a Group 1 carcinogen by the International Agency for Research on Cancer in 2013 and is an emerging global environmental risk factor that is a major cause of death related to cardiovascular and respiratory diseases. PM is a complex composed of highly reactive organic matter, chemicals, and metal components, which mainly cause excessive production of reactive oxygen species (ROS) that can lead to DNA and cell damage, endoplasmic reticulum stress, inflammatory responses, atherosclerosis, and airway remodeling, contributing to an increased susceptibility to and the exacerbation of various diseases and infections. PM has various effects on human health depending on the particle size, physical and chemical characteristics, source, and exposure period. PM smaller than 5 mum can penetrate and accumulate in the alveoli and circulatory system, causing harmful effects on the respiratory system, cardiovascular system, skin, and brain. In this review, we describe the relationship and mechanism of ROS-mediated cell damage, oxidative stress, and inflammatory responses caused by PM and the health effects on major organs, as well as comprehensively discuss the harmfulness of PM.
Autores: Varricchi G, Brightling CE, Grainge C, et al.
Publicación: 18 Abril 2024
Remodelación de las vías respiratorias en el asma y el epitelio: al borde de una nueva era
Abstract
Asthma is a chronic, heterogeneous disease of the airways, often characterised by structural changes known collectively as airway remodelling. In response to environmental insults, including pathogens, allergens and pollutants, the epithelium can initiate remodelling via an inflammatory cascade involving a variety of mediators that have downstream effects on both structural and immune cells. These mediators include the epithelial cytokines thymic stromal lymphopoietin, interleukin (IL)-33 and IL-25, which facilitate airway remodelling through cross-talk between epithelial cells and fibroblasts, and between mast cells and airway smooth muscle cells, as well as through signalling with immune cells such as macrophages. The epithelium can also initiate airway remodelling independently of inflammation in response to the mechanical stress present during bronchoconstriction. Furthermore, genetic and epigenetic alterations to epithelial components are believed to influence remodelling. Here, we review recent advances in our understanding of the roles of the epithelium and epithelial cytokines in driving airway remodelling, facilitated by developments in genetic sequencing and imaging techniques. We also explore how new and existing therapeutics that target the epithelium and epithelial cytokines could modify airway remodelling.
Autores: Vianello A, Guarnieri G, Achille A, et al.
Publicación: 30 Marzo 2024
Biomarcadores séricos de remodelación en el asma grave con obstrucción fija de las vías respiratorias y el papel potencial del KL-6
Abstract
Over 3% of asthmatic patients are affected by a particularly severe form of the disease ("severe asthma", SA) which is often refractory to standard treatment. Airway remodeling (AR), which can be considered a critical characteristic of approximately half of all patients with SA and currently thought to be the main mechanism triggering fixed airway obstruction (FAO), seems to be a key factor affecting a patient's outcome. Despite the collective efforts of internationally renowned experts, to date only a few biomarkers indicative of AR and no recognizable biomarkers of lung parenchymal remodeling have been identified. This work examines the pathogenesis of airway and lung parenchymal remodeling and the serum biomarkers that may be able to identify the severe asthmatic patients who may develop FAO. The study also aims to examine if Krebs von den Lungen-6 (KL-6) could be considered a diagnostic biomarker of lung structural damage in SA.
ES-41206 Marzo 2026
Autores: Spector C, De Sanctis CM, Panettieri RA, et al.
Publicación: 29 Septiembre 2023
El rinovirus induce remodelación de las vías respiratorias: ¿cuáles son las consecuencias fisiológicas?
Abstract
BACKGROUND: Rhinovirus infections commonly evoke asthma exacerbations in children and adults. Recurrent asthma exacerbations are associated with injury-repair responses in the airways that collectively contribute to airway remodeling. The physiological consequences of airway remodeling can manifest as irreversible airway obstruction and diminished responsiveness to bronchodilators. Structural cells of the airway, including epithelial cells, smooth muscle, fibroblasts, myofibroblasts, and adjacent lung vascular endothelial cells represent an understudied and emerging source of cellular and extracellular soluble mediators and matrix components that contribute to airway remodeling in a rhinovirus-evoked inflammatory environment.
MAIN BODY: While mechanistic pathways associated with rhinovirus-induced airway remodeling are still not fully characterized, infected airway epithelial cells robustly produce type 2 cytokines and chemokines, as well as pro-angiogenic and fibroblast activating factors that act in a paracrine manner on neighboring airway cells to stimulate remodeling responses. Morphological transformation of structural cells in response to rhinovirus promotes remodeling phenotypes including induction of mucus hypersecretion, epithelial-to-mesenchymal transition, and fibroblast-to-myofibroblast transdifferentiation. Rhinovirus exposure elicits airway hyperresponsiveness contributing to irreversible airway obstruction. This obstruction can occur as a consequence of sub-epithelial thickening mediated by smooth muscle migration and myofibroblast activity, or through independent mechanisms mediated by modulation of the β2 agonist receptor activation and its responsiveness to bronchodilators. Differential cellular responses emerge in response to rhinovirus infection that predispose asthmatic individuals to persistent signatures of airway remodeling, including exaggerated type 2 inflammation, enhanced extracellular matrix deposition, and robust production of pro-angiogenic mediators.
CONCLUSIONS: Few therapies address symptoms of rhinovirus-induced airway remodeling, though understanding the contribution of structural cells to these processes may elucidate future translational targets to alleviate symptoms of rhinovirus-induced exacerbations.
ES-41206 Marzo 2026
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