Megakaryocytes (MKs) are typical cellular components in the circulating blood flowing from the heart into the lungs. Physiologically, MKs function as an important regulator of platelet production and immunoregulation. However, dysfunction in MKs is considered a trigger in various diseases. It has been described that the lung is an important site of platelet biogenesis from extramedullary MKs, which may play an essential role in various pulmonary diseases. With detailed studies, there are different degrees of numerical changes of MKs in coronavirus disease 2019 (COVID-19), acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), lung cancer, pulmonary fibrosis (PF), and other pulmonary diseases. Also, MKs inhibit or promote the development of pulmonary diseases through various pathways. Here, we summarize the current knowledge of MKs in pulmonary diseases, highlighting the physiological functions and integrated molecular mechanisms. We aim to shine new light on not only the subsequent study of MKs but also the diagnosis and treatment of pulmonary diseases.
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http://dx.doi.org/10.1016/j.lfs.2022.120602 | DOI Listing |
Respir Res
January 2025
School of Engineering, University of Warwick, Coventry, CV4 7AL, UK.
Introduction And Objectives: High flow nasal cannula (HFNC) therapy is an increasingly popular mode of non-invasive respiratory support for the treatment of patients with acute hypoxemic respiratory failure (AHRF). Previous experimental studies in healthy subjects have established that HFNC generates flow-dependent positive airway pressures, but no data is available on the levels of mean airway pressure (mP) or positive end-expiratory pressure (PEEP) generated by HFNC therapy in AHRF patients. We aimed to estimate the airway pressures generated by HFNC at different flow rates in patients with AHRF, whose functional lung volume may be significantly reduced compared to healthy subjects due to alveolar consolidation and/or collapse.
View Article and Find Full Text PDFRespir Res
January 2025
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Background: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease, influenced by both environmental and genetic factors. Single nucleotide polymorphism (SNP) in the human genome may influence the risk of developing COPD and the response to treatment. We assessed the effects of gene polymorphism of inflammatory and immune-active factors and gene-environment interaction on risk of COPD in middle-aged and older Chinese individuals.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, Warsaw, 02-097, Poland.
Background: Pathobiology of asthma and chronic obstructive pulmonary disease (COPD) is associated with changes among respiratory epithelium structure and function. Increased levels of PM from urban particulate matter (UPM) are correlated with enlarged rate of asthma and COPD morbidity as well as acute disease exacerbation. It has been suggested that pre-existing pulmonary obstructive diseases predispose epithelium for different biological response than in healthy airways.
View Article and Find Full Text PDFBMC Cancer
January 2025
Finetech in Medicine Research Center, Iran University of Medical Sciences, Tehran, Iran.
Background And Aim: Zinc oxide and copper oxide nanoparticles are known for their promising biological activities. This study aims to synthesize zinc oxide nanoparticles and copper-doped zinc oxide nanoparticles to harness the combined cytotoxic and anticancer effects of them in vitro and in vivo studies.
Methods: Zinc oxide nanoparticles, both doped and undoped, were synthesized using a chemical co-precipitation method.
Nat Immunol
January 2025
Department of Medicine, Department of Pathology, Department of Microbiology & Immunology, McGill University Health Centre, McGill International TB Centre, Meakins Christie Laboratories, McGill University, Montréal, Québec, Canada.
Disease tolerance is an evolutionarily conserved host defense strategy that preserves tissue integrity and physiology without affecting pathogen load. Unlike host resistance, the mechanisms underlying disease tolerance remain poorly understood. In the present study, we investigated whether an adjuvant (β-glucan) can reprogram innate immunity to provide protection against influenza A virus (IAV) infection.
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