Abstract
Impaired endothelial cell (EC) growth and function have been proposed to be an initial event that leads to the development of atherosclerosis. There is a growing body of evidence that atherosclerosis is an inflammatory-fibroproliferative disease, and ECs are target for cytokines and growth factors released during inflammation. Recently, nifedipine, one of the most widely used dihydropyridine-based calcium antagonists (DHPs) for treatments of patients with hypertension, was shown to inhibit vascular inflammation and subsequently improve endothelial function in many cardiovascular diseases, thus slowing the development and progression of atherosclerosis. However, the molecular mechanisms underlying this are not fully understood, because ECs do not possess voltage-operated L-type calcium channels. In this review, we discuss the pleiotropic effects of nifedipine on atherosclerosis, especially focusing on its anti-oxidative properties.
| Original language | English |
|---|---|
| Pages (from-to) | 1543-1547 |
| Number of pages | 5 |
| Journal | Current Pharmaceutical Design |
| Volume | 12 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - 2006 Apr |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Advanced glycation end products
- Atherosclerosis
- Diabetes
- Insulin resistance
- Nitric oxide
- Oxidative stress
ASJC Scopus subject areas
- Pharmacology
- Drug Discovery
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