Abstract
Myocardial infarction and adverse postinfarct remodeling in older persons lead to poor outcome and need greater understanding of the contributions of age-related factors on abnormal cardiac function and management. In this perspective, how normal aging processes could contribute to the events of post-myocardial infarction and remodeling is reviewed. Post-myocardial infarction and remodeling involve cardiomechanical factors and neurohormonal response. Many factors prevent or accelerate aging including immunosenescence, recruitment and regeneration of stem cells, telomere shortening, oxidative damage, antiaging hormones klotho and melatonin, nutrition, and Sirtiun protein family, and these factors could affect post-MI remodeling and heart failure. Interest in stem cell repair of myocardial infarcts to mitigate post-MI remodeling needs more information on aging of stem cells, and potential effects on stem cell use in infarct repair. Integrating genomics and proteomics methods may help find clinically novel therapy in the management of post-MI remodeling and heart failure in aged individuals.
Highlights
Aging is universal and is governed by may factors, the basis of which many be theoretical
The present paper aims to summarize relevant ideas of normal aging process and factors involved in promoting or protecting tissue and organ aging
The changes in cardiac function and morphology with aging before onset of myocardial infarction (MI), myocardial infarction and remodeling and effects of aging factors and the search for ways to ameliorate the adverse outcome of postMI remodeling in older individuals including use of “stem cells” for infarct repair
Summary
Aging is universal and is governed by may factors, the basis of which many be theoretical. The fundamental argument is whether aging is programmed or determined by interactions between environmental and genetic factors [1] (Table 1). Many are searching for human longevity genes but the efforts are complicated or compounded by the role of interdependent environmental factors. Centenarian offsprings have longer telomeres and their experience suggests close interaction of environment and cellular repair systems[8]. Model systems have provided a wealth of information on the roles of altered genetic factors on aging [9]. The changes in cardiac function and morphology with aging before onset of myocardial infarction (MI), myocardial infarction and remodeling and effects of aging factors and the search for ways to ameliorate the adverse outcome of postMI remodeling in older individuals including use of “stem cells” for infarct repair
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