"Vulnerable plaques" - Ticking of the time bomb

Amit K. Mitra, Ashwini S. Dhume, Devendra K. Agrawal

    Research output: Contribution to journalArticlepeer-review

    28 Scopus citations

    Abstract

    Atherosclerosis and its sequelae are one of the leading causes of morbidity and mortality, especially in the developed nations. Over the years, treatment protocols have changed with the changing understanding of the disease process. Inflammatory mechanisms have emerged as key players in the formation of the atherosclerotic plaque. For the majority of its life span, the plaque develops silently and only some exhibit overt clinical manifestations. The purpose of this review is to examine the inherent properties of some of these "vulnerable" or symptomatic plaques. Rupture of the plaque is related to the thickness of the fibrous cap overlying the necrotic lipid core. A thin cap is more likely to lead to rupture. Multiple factors broadly grouped as the "determinants of vulnerability" are responsible for directly or indirectly influencing the plaque dynamics. Apoptosis is considered an important underlying mechanism that contributes to plaque instability. Inflammatory reactions within the plaque trigger apoptosis by cell-cell contact and intracellular death signaling. Once started, the apoptotic process affects all of the components that make up the plaque, including vascular smooth muscle cells, endothelial cells, and macrophages. Extensive research has identified many of the key cellular and molecular regulators that play a part in apoptosis within the atherosclerotic lesion. This information will help us to gain a better understanding of the underlying mechanisms at the cellular and molecular level and enable us to formulate better therapeutic strategies to combat this disease.

    Original languageEnglish
    Pages (from-to)860-871
    Number of pages12
    JournalCanadian Journal of Physiology and Pharmacology
    Volume82
    Issue number10
    DOIs
    StatePublished - Oct 2004

    All Science Journal Classification (ASJC) codes

    • Physiology
    • Pharmacology

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