Publications by authors named "Manuela Marega"

Article Synopsis
  • Fibrosis, especially idiopathic pulmonary fibrosis (IPF), is linked to abnormal healing processes in the lungs that can lead to organ failure, with no current cure.
  • The study investigates activated myofibroblasts (aMYFs), their different subtypes, and their roles in lung repair and damage using genetic and transcriptomic analysis in mice, as well as human data.
  • Findings reveal that aMYFs can be categorized into four distinct groups, with a specific subset linked to both the progression and resolution of fibrosis, suggesting new potential treatment targets for managing IPF.
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Myofibroblasts (MYFs) are generally considered the principal culprits in excessive extracellular matrix deposition and scar formation in the pathogenesis of lung fibrosis. Lipofibroblasts (LIFs), on the other hand, are defined by their lipid-storing capacity and are predominantly found in the alveolar regions of the lung. They have been proposed to play a protective role in lung fibrosis.

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease commonly seen in preterm infants, and is triggered by infection, mechanical ventilation, and oxygen toxicity. Among other problems, lifelong limitations in lung function and impaired psychomotor development may result. Despite major advances in understanding the disease pathologies, successful interventions are still limited to only a few drug therapies with a restricted therapeutic benefit, and which sometimes have significant side effects.

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The adult human lung is constantly exposed to irritants like particulate matter, toxic chemical compounds, and biological agents (bacteria and viruses) present in the external environment. During breathing, these irritants travel through the bronchi and bronchioles to reach the deeper lung containing the alveoli, which constitute the minimal functional respiratory units. The local biological responses in the alveoli that follow introduction of irritants need to be tightly controlled in order to prevent a massive inflammatory response leading to loss of respiratory function.

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