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Angiotensin II in apoptotic lung injury: potential role in meconium aspiration syndrome
1Department of Physiology, Michigan State University, East Lansing, MI 48824, USA. uhal@msu.edu
Abstract:
Meconium aspiration injures a number of cell types in the lung, most notably airway and alveolar epithelial lining cells. Recent data show that at least some of the cell death induced by meconium occurs by apoptosis, and therefore has the potential for pharmacologic inhibition through the use of apoptosis blockers or other strategies. Related work in adult animal models of lung injury has shown that apoptosis of lung epithelial cells induces a local (that is, entirely lung tissue specific) renin-angiotensin system (RAS(L)). Furthermore, this inducible RAS(L) is required for the apoptotic response and affects other adjacent cell types through the release of angiotensin II and related peptides. This manuscript reviews the published data supporting this viewpoint as well as more recent works that suggest the involvement of a RAS(L) in the perinatal lung damage associated with meconium aspiration syndrome (MAS). The implications of these findings regarding their potential for the clinical management of MAS are also discussed.
Insights
Meconium aspiration causes lung cell death via apoptosis, potentially involving a local renin-angiotensin system (RAS(L)). This review explores RAS(L) involvement in meconium aspiration syndrome (MAS) and its clinical implications.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pharmacology
Background:
- Meconium aspiration syndrome (MAS) causes lung injury, primarily affecting airway and alveolar epithelial cells.
- Cell death in MAS can occur via apoptosis, suggesting potential for pharmacologic intervention.
- Previous research indicates apoptosis in adult lung injury models induces a local renin-angiotensin system (RAS(L)).
Purpose of the Study:
- To review evidence supporting the role of RAS(L) in meconium-induced lung injury.
- To discuss the potential clinical implications of RAS(L) involvement in MAS management.
Main Methods:
- Review of published data on apoptosis and RAS(L) in lung injury.
- Analysis of recent findings linking RAS(L) to perinatal lung damage in MAS.
Main Results:
- Apoptosis of lung epithelial cells can induce a lung-specific renin-angiotensin system (RAS(L)).
- This inducible RAS(L) is crucial for the apoptotic process and impacts adjacent cells via angiotensin II.
- Emerging evidence suggests RAS(L) involvement in the lung damage seen in meconium aspiration syndrome (MAS).
Conclusions:
- The local renin-angiotensin system (RAS(L)) may play a significant role in the pathophysiology of meconium aspiration syndrome (MAS).
- Understanding the RAS(L) pathway offers potential new therapeutic targets for managing MAS in neonates.
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