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Involvement of the ADAM 12 in thrombin-induced rat's VSMCs proliferation
K Smiljanic1, B Dobutovic, M Obradovic
1University of Belgrade, Laboratory for Molecular Genetics and Radiobiology, Institute Vinca P.O. Box 522, 11000 Belgrade, Serbia. katicas71@gmail.com
Insights
Thrombin (Thr) drives vascular smooth muscle cell (VSMC) proliferation in cardiovascular diseases. This review highlights ADAM 12
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Vascular Pathophysiology
Background:
- Cardiovascular disease, primarily atherosclerosis, is a leading cause of mortality.
- Vascular smooth muscle cell (VSMC) proliferation is central to atherosclerosis and hypertension pathogenesis.
- Thrombin (Thr) significantly contributes to abnormal VSMC proliferation in these conditions.
Purpose of the Study:
- To review signaling mechanisms of Thr-induced VSMC proliferation.
- To emphasize the role of ADAM 12 in VSMC hypertrophy and vascular diseases.
- To enhance understanding of Thr's role in vascular biology and disease.
Main Methods:
- Literature review of recent findings on signaling pathways.
- Focus on the involvement of ADAM metalloproteinases, specifically ADAM 12.
- Analysis of Thr-mediated regulation of VSMC proliferation.
Main Results:
- Thrombin (Thr) activates signaling pathways that promote VSMC proliferation.
- ADAM 12 is identified as a key mediator in Thr-induced VSMC hypertrophy.
- ADAM metalloproteinase activity is present in Thr-induced VSMC proliferation.
Conclusions:
- Thrombin (Thr) plays a critical role in VSMC proliferation via specific signaling pathways.
- ADAM 12 is a significant mediator of VSMC hypertrophy and vascular disease development.
- Understanding these mechanisms is crucial for developing therapeutic strategies against cardiovascular diseases.
Abstract:
Cardiovascular disease is the largest single cause of mortality and its major underlying pathology is atherosclerosis. The proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of the various vascular diseases, including atherosclerosis and hypertension. Thrombin (Thr) is involved in the abnormal proliferation of VSMCs associated with atherosclerosis and hypertension. ADAMs (A Disintegrin And Metalloproteinase) are transmembrane metalloproteinases, belonging to the adamalysins group, that are distinct from matrix metalloproteinases (MMPs) in a way as they have an extracellular disintegrin domain and cytoplasmic domain that can associate with intracellular proteins. There is limited knowledge about the presence of ADAM metalloproteinase activity in Thr-induced VSMCs proliferation. Therefore, this review examines recent findings in signaling mechanisms employed by Thr in modulating the regulation of proliferation of VSMCs with particular emphasis on involvement of ADAM 12 which has been identified as an important mediator of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of Thr in vascular biology and vascular diseases.
