AI Article Synopsis
- Idiopathic pulmonary fibrosis (IPF) mainly affects patients over 65, with several recently identified risk factors, though its exact cause is still unknown.
- The abnormal lung structure in IPF, combined with activated fibroblasts, leads to hypoxia and promotes the production of exosomes that are involved in cell communication.
- The study explores how hypoxic conditions influence the contents of exosomes and their role in changing fibroblast metabolism during the progression of IPF, a topic that needs further investigation.
Article Abstract
Idiopathic pulmonary fibrosis (IPF) has a high incidence and prevalence among patients over 65 years old. While its exact etiology remains unknown, several risk factors have recently been identified. Hypoxia is associated with IPF due to the abnormal architecture of lung parenchyma and the accumulation of extracellular matrix produced by activated fibroblasts. Exosomes play a crucial role in intercellular communication during both physiological and pathological processes, including hypoxic diseases like IPF. Recent findings suggest that a hypoxic microenvironment influences the content of exosomes in various diseases, thereby altering cellular metabolism. Although the role of exosomes in IPF is an emerging area of research, the significance of hypoxic exosomes as inducers of metabolic reprogramming in fibroblasts is still underexplored. In this study, we analyze and discuss the relationship between hypoxia, exosomal cargo, and the metabolic reprogramming of fibroblasts in the progression of IPF.
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| http://dx.doi.org/10.1016/j.biopha.2024.117680 | DOI Listing |
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