File:Pulmonary and cardiovascular dysfunction and their cellular basis.png
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| Description | Summary of pulmonary and cardiovascular dysfunction and their cellular basis. (a) EC use has been linked to disease and dysfunction in the heart and lungs. (b) i. Platelets are activated towards a pro-thrombotic phenotype in the vessel; ii. ECA exposure promotes endothelial cell death and compromised barrier function, which facilitates immune cell extravasation into the surrounding tissue. Endothelial cells release inflammatory cytokines that enhance neutrophil recruitment; iii. Monocytes differentiate into macrophages upon extravasation. Neutrophils and macrophages remodel extracellular matrix in the interstitium as an inflammatory response, promoting compromise of the epithelium and endothelium; iv. Epithelial permeability is compromised and ECA exposure is associated with epithelial cell apoptosis and necrosis; v. ECA exposed macrophages and neutrophils enter the lung tissue and promote inflammation. Macrophages take up EC-associated lipids. Not to scale. |
| Date | |
| Source | https://www.mdpi.com/1422-0067/22/22/12452 |
| Author | Hunter T. Snoderly, Timothy R. Nurkiewicz, Elizabeth C. Bowdridge, Margaret F. Bennewitz |
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| Date/Time | Thumbnail | Dimensions | User | Comment | |
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| current | 10:09, 26 February 2024 | | 3,664 × 2,120 (812 KB) | Ameisenigel (talk | contribs) | {{Information |Description=Summary of pulmonary and cardiovascular dysfunction and their cellular basis. (a) EC use has been linked to disease and dysfunction in the heart and lungs. (b) i. Platelets are activated towards a pro-thrombotic phenotype in the vessel; ii. ECA exposure promotes endothelial cell death and compromised barrier function, which facilitates immune cell extravasation into the surrounding tissue. Endothelial cells release inflammatory cytokines that enhance neutrophil recr... |
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