| Autor: |
O'Callaghan M; Department of Respiratory Medicine, St. Vincent's University Hospital, Dublin, Ireland.; School of Medicine, University College Dublin, Dublin, Ireland., Tarling EJ; Division of Cardiology, University of California, Los Angeles, Los Angeles, California; and., Bridges JP; Department of Medicine and., Redente EF; Department of Pediatrics, National Jewish Health, Denver, Colorado., Byrne AJ; School of Medicine, University College Dublin, Dublin, Ireland., Keane MP; Department of Respiratory Medicine, St. Vincent's University Hospital, Dublin, Ireland.; School of Medicine, University College Dublin, Dublin, Ireland., McCarthy C; Department of Respiratory Medicine, St. Vincent's University Hospital, Dublin, Ireland.; School of Medicine, University College Dublin, Dublin, Ireland. |
| Abstrakt: |
Pulmonary fibrosis (PF) can be idiopathic or driven by a specific insult, genetic susceptibility, or disease process. Inflammation plays a role in the pathophysiology, the extent of which remains a longstanding topic of debate. More recently, there has been increasing interest in a potential inciting role for aberrant lipid metabolism. Lipids are essential for the structure and function of all cell membranes, but specifically in the lung for surfactant composition, intra- and intercellular lipid mediators, and lipofibroblasts. Clinically, there is evidence of increased lipid deposition in the subpleural space and at a whole-lung tissue level in PF. There is evidence of increased parenchymal lipid deposition and abnormal mediastinal fat shape on chest computed tomography. A protective role for cholesterol-lowering drugs, including statins and ezetimibe, has been described in PF. At a cellular level, fatty acid, phospholipid, and glucose metabolism are disordered, as is the production of lipid mediators. Here we put forward the argument that there is substantive clinical and biological evidence to support a role for aberrant lipid metabolism and lipid mediators in the pathogenesis of PF. |
