Abstract
Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart. However, the mechanism of mitochondria-mediated apoptosis in aged hearts remains poorly understood. Here, we used male Fischer 344 rats of various ages, representing very young (1 month), young (4 months), middle-aged (12 months), and old (20 months) rats, to determine whether mitochondria-mediated apoptotic signals and apoptosis in the left ventricle of the heart are altered notably with aging. As the rats aged, the extramyocyte space and myocyte cross-sectional area in their left ventricle muscle increased, while the number of myocytes decreased. Additionally, mitochondrion-mediated apoptotic signals and apoptosis increased remarkably during aging. Therefore, our results demonstrate that aging promotes remarkable morphological changes and increases the degree of mitochondrion-mediated apoptosis in the left ventricle of rat hearts.
Highlights
Aging is commonly characterized by a gradual deterioration of tissue and organ function, and has been identified as the main cause of cardiac dysfunction
To distinguish the alterations that occur during biological aging, we investigated the changes in the myocardial structure and mitochondria-mediated apoptotic signaling in the cardiac muscles of male
Cardiac muscle remodeling was determined by measuring extramyocyte space, extent of apparent fibrosis, myocyte cross-sectional area (CSA), and the number of myocytes per 100,000 μm2 (Figure 1A)
Summary
Aging is commonly characterized by a gradual deterioration of tissue and organ function, and has been identified as the main cause of cardiac dysfunction. Aging causes significant alterations in the structure and function of the heart, especially in the left ventricle, in addition to increasing cardiac oxidative stress and inflammation [1,3]. Impaired cardiac structure and function with aging result in enhanced susceptibility to cardiovascular diseases (such as heart failure), which can contribute to morbidity and mortality. Mitochondria are the energy power plants of cells, controlling their fate. They are an important player in various processes and have the ability to maintain metabolic homeostasis and manage aging-related mechanisms [2]. Several studies suggested that mitochondria have evolved to regulate other cellular functions, including those contributing to biological aging, such as the generation of reactive oxygen species (ROS), inflammation, senescence, and resultant necrotic and apoptotic cell death [4]. Our studies have revealed that aging mainly results in damage to the electron transport chain during mitochondrial respiration, due to a decrease in electron transport by complex II-IV, which can promote electron leakage and ROS production [5]
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