Effect of nicotine on the cardiac aging process
Abstracts
Initial Award Abstract |
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With increased age, people are more likely to suffer a heart attack, a stroke, or to develop coronary heart disease and heart failure. Cardiovascular diseases are also a major cause of disability, reducing the quality of life for millions of older people. Smoking is also a well-known risk factor for developing heart disease and recent studies suggest that a link exists between smoking and aging. In fact, the World Health Organization has reported that smokers show patterns of accelerated aging. The use of nicotine replacements such as e-cigarettes has increased significantly in the US in recent years. Although e-cigarettes lack the harmful chemical products of tobacco smoke, the potential negative effects on human health with long-term exposure to nicotine are still unclear. The muscle cells in the heart contains lot of mitochondria that are responsible for providing energy to ensure continuous contraction of the heart. When mitochondria become old or damaged, they are rapidly removed via an important cellular quality control pathway called autophagy. In this process, damaged mitochondria are sequestered by vesicles called autophagosomes which subsequently deliver the mitochondria to lysosomes where they are degraded. When this process is impaired, it can lead to accumulation of damaged mitochondria and loss of muscle cells. This, in turn, can result in development of heart failure. It is known that this process is reduced in various tissues with age. In this proposal, I will explore how aging and chronic nicotine exposure affect autophagy in the heart. In addition, I will investigate whether long-term nicotine exposure functions as a cardiac aging accelerator. My study will provide a better understanding of the effects that nicotine will have on the heart and potential role in cardiovascular disease. |
