Injured lung endothelium: mechanisms of self-repair and agonist-assisted recovery (2017 Grover Conference Series)
The lung endothelium is vulnerable to both exogenous and endogenous insults, so a properly coordinated efficient repair system is essential for the timely recovery of the lung after injury. The agents that cause endothelial injury and dysfunction fall into a broad range from mechanical forces such a...
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| Format: | Article |
| Language: | English |
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Wiley
2018-02-01
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| Series: | Pulmonary Circulation |
| Online Access: | https://doi.org/10.1177/2045893217752660 |
| _version_ | 1811228231005634560 |
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| author | Konstantin G. Birukov Pratap Karki |
| author_facet | Konstantin G. Birukov Pratap Karki |
| author_sort | Konstantin G. Birukov |
| collection | DOAJ |
| description | The lung endothelium is vulnerable to both exogenous and endogenous insults, so a properly coordinated efficient repair system is essential for the timely recovery of the lung after injury. The agents that cause endothelial injury and dysfunction fall into a broad range from mechanical forces such as pathological cyclic stretch and shear stress to bacterial pathogens and their virulent components, vasoactive agonists including thrombin and histamine, metabolic causes including high glucose and oxidized low-density lipoprotein (OxLDL), circulating microparticles, and inflammatory cytokines. The repair mechanisms employed by endothelial cells (EC) can be broadly categorized into three groups: (1) intrinsic mechanism of recovery regulated by the cross-talk between small GTPases as exemplified by Rap1-mediated EC barrier recovery from Rho-mediated thrombin-induced EC hyperpermeability; (2) agonist-assisted recovery facilitated by the activation of Rac and Rap1 with subsequent inhibition of Rho signaling as observed with many barrier protective agonists including oxidized phospholipids, sphingosine 1-phosphate, prostacyclins, and hepatocyte growth factor; and (3) self-recovery of EC by the secretion of growth factors and other pro-survival bioactive compounds including anti-inflammatory molecules such as lipoxins during the resolution of inflammation. In this review, we will discuss the molecular and cellular mechanisms of pulmonary endothelium repair that is critical for the recovery from various forms of lung injuries. |
| first_indexed | 2024-04-12T09:55:52Z |
| format | Article |
| id | doaj.art-cc58e9d8d94c4c8692f025d0ebca934f |
| institution | Directory Open Access Journal |
| issn | 2045-8940 |
| language | English |
| last_indexed | 2024-04-12T09:55:52Z |
| publishDate | 2018-02-01 |
| publisher | Wiley |
| record_format | Article |
| series | Pulmonary Circulation |
| spelling | doaj.art-cc58e9d8d94c4c8692f025d0ebca934f2022-12-22T03:37:43ZengWileyPulmonary Circulation2045-89402018-02-01810.1177/2045893217752660Injured lung endothelium: mechanisms of self-repair and agonist-assisted recovery (2017 Grover Conference Series)Konstantin G. Birukov0Pratap Karki1Department of Anesthesiology, University of Maryland Baltimore, School of Medicine, Baltimore, MD, USADivision of Pulmonary and Critical Care Medicine, Department of Medicine, University of Maryland Baltimore, School of Medicine, Baltimore, MD, USAThe lung endothelium is vulnerable to both exogenous and endogenous insults, so a properly coordinated efficient repair system is essential for the timely recovery of the lung after injury. The agents that cause endothelial injury and dysfunction fall into a broad range from mechanical forces such as pathological cyclic stretch and shear stress to bacterial pathogens and their virulent components, vasoactive agonists including thrombin and histamine, metabolic causes including high glucose and oxidized low-density lipoprotein (OxLDL), circulating microparticles, and inflammatory cytokines. The repair mechanisms employed by endothelial cells (EC) can be broadly categorized into three groups: (1) intrinsic mechanism of recovery regulated by the cross-talk between small GTPases as exemplified by Rap1-mediated EC barrier recovery from Rho-mediated thrombin-induced EC hyperpermeability; (2) agonist-assisted recovery facilitated by the activation of Rac and Rap1 with subsequent inhibition of Rho signaling as observed with many barrier protective agonists including oxidized phospholipids, sphingosine 1-phosphate, prostacyclins, and hepatocyte growth factor; and (3) self-recovery of EC by the secretion of growth factors and other pro-survival bioactive compounds including anti-inflammatory molecules such as lipoxins during the resolution of inflammation. In this review, we will discuss the molecular and cellular mechanisms of pulmonary endothelium repair that is critical for the recovery from various forms of lung injuries.https://doi.org/10.1177/2045893217752660 |
| spellingShingle | Konstantin G. Birukov Pratap Karki Injured lung endothelium: mechanisms of self-repair and agonist-assisted recovery (2017 Grover Conference Series) Pulmonary Circulation |
| title | Injured lung endothelium: mechanisms of self-repair and agonist-assisted
recovery (2017 Grover Conference Series) |
| title_full | Injured lung endothelium: mechanisms of self-repair and agonist-assisted
recovery (2017 Grover Conference Series) |
| title_fullStr | Injured lung endothelium: mechanisms of self-repair and agonist-assisted
recovery (2017 Grover Conference Series) |
| title_full_unstemmed | Injured lung endothelium: mechanisms of self-repair and agonist-assisted
recovery (2017 Grover Conference Series) |
| title_short | Injured lung endothelium: mechanisms of self-repair and agonist-assisted
recovery (2017 Grover Conference Series) |
| title_sort | injured lung endothelium mechanisms of self repair and agonist assisted recovery 2017 grover conference series |
| url | https://doi.org/10.1177/2045893217752660 |
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