Extracellular matrix remodeling in the post-myocardial infarction aging heart

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, SA47

Research Symposium: Extracellular matrix remodeling in the post-myocardial infarction aging heart

A. Yabluchanskiy1,3, Y. Ma1, Y. Jin2, M. Lindsey1,3

1. Physiology & Biophysics, Univ MS Medical Center, Jackson, Mississippi, United States. 2. Electrical and Computer Engineering, UTSA, San Antonio, Texas, United States. 3. Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, Mississippi, United States.

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Aging impairs the ability of the left ventricle (LV) to respond to stress or injury. Cardiac aging is characterized by increased inflammation, an accumulation of extracellular matrix (ECM), and the development of diastolic dysfunction. Matrix metalloproteinases (MMPs) are key enzymes that regulate ECM turnover, and in particular MMP-9 deletion has been shown to attenuate LV dysfunction and remodeling post-myocardial infarction (MI) in young mice, by coordinating inflammatory and ECM responses. MMP-9 levels rise with age, in both the LV and plasma. The increase in cardiac MMP-9 is due to an accumulation of macrophages, which contribute to the increase in inflammation and ECM. Aging, therefore, gradually resets the cardiac environment. This talk will discuss the outcomes when myocardial infarction (MI) is superimposed on a cardiac aging background, focusing on changes to the inflammatory response that coordinate infarct scar formation and how MMP-9 deletion regulates these changes in the aging setting.



Where applicable, experiments conform with Society ethical requirements.

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