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09:18
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
[Apoptosis and acute coronary syndromes]
1Inserm U.541, Hôpital Lariboisière, 75475 Paris Cedex 10, France.
Medecine Sciences : M/S
|April 7, 2004
Summary
Atherosclerosis involves arterial wall inflammation. Inflammatory mediators and apoptosis contribute to plaque rupture and thrombus formation, causing ischemic events.
Area of Science:
- Cardiovascular Biology
- Inflammation Research
- Pathology
Context:
- Atherosclerosis is a chronic inflammatory arterial disease.
- Ischemic events stem from thrombus formation on unstable plaques.
- Plaque instability is linked to endothelial erosion or fibrous cap rupture.
Purpose:
- To explore the roles of inflammation and apoptosis in atherosclerotic plaque destabilization.
- To understand the mechanisms leading to plaque rupture and thrombus formation.
Summary:
- Inflammatory processes, driven by pro-inflammatory mediators, contribute to smooth muscle cell loss and collagen degradation, weakening the fibrous cap.
- Apoptosis (programmed cell death) is identified as a key factor increasing plaque thrombogenicity.
- Plaque rupture (60%) and erosion (40%) are the primary triggers for thrombus formation in atherosclerosis.
Impact:
- Highlights the critical involvement of inflammatory and apoptotic pathways in atherosclerotic cardiovascular disease.
- Provides insights into molecular mechanisms underlying plaque instability and thrombotic events.
- Informs potential therapeutic strategies targeting inflammation and apoptosis to prevent ischemic complications.
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