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Advances in Pulmonary Fibrosis: Beyond the Fibroblast

Advances in Translational Models to Study Fibrosis
Reported by
Sara Donnelly

Posted May 28, 2020

Presented By

Biochemical Pharmacology Discussion Group

The New York Academy of Sciences


Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease with few treatment options. Research on IPF and other interstitial lung diseases has historically focused on fibroblasts and the importance of TGF-beta-driven epithelial to mesenchymal transition. Recently, new data have highlighted key roles for additional cell types, including alveolar epithelial cells and endothelial cells, in the development or maintenance of lung fibrosis. Moreover, cellular senescence and immune pathways have also been found to contribute to IPF pathogenesis. This eBriefing showcases emerging biological mechanisms underlying the etiology of pulmonary fibrosis and explores novel ways to remove, repair or regenerate damaged lung.

In This eBriefing, You’ll Learn

  • The importance of cellular senescence and immune signaling in IPF
  • The roles of endothelial cells and alveolar epithelial cells, which are emerging as key drivers of disease
Identifying Therapeutic Targets in Pulmonary Fibrosis
Can Altering Myofibroblast Cell Fate in Aging Promote Youthful Healing?
Senolytics as Potential Disease Modifiers in Idiopathic Pulmonary Fibrosis
Mitochondrial Dysfunction And Aging At The Crossroad Of The Pathogenesis Of Lung Fibrosis
Role of Bronchial Epithelial Cells in Alveolar Epithelial Regeneration in Lung Fibrosis
Sex Specific Inhibition of pSTAT3 Signaling in Programmed Death (PD)-1+ CD4+ T Cells Reduces Lung Fibrosis Pathogenesis
Mechanisms Regulating the Recruitment of Monocyte-Derived Macrophages During Pulmonary Fibrosis
There Is Nothing Beyond the Fibroblast - On This Flat Earth