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The Role of Apoptosis in the Normal Aging Brain, Skeletal Muscle, and Heart
Author(s) -
POLLACK MICHAEL,
PHANEUF SHARON,
DIRKS AMIE,
LEEUWENBURGH CHRISTIAAN
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb02086.x
Subject(s) - apoptosis , mitochondrion , cytochrome c , mitochondrial permeability transition pore , skeletal muscle , microbiology and biotechnology , oxidative stress , biology , myocyte , mitochondrial apoptosis induced channel , programmed cell death , endocrinology , biochemistry
During aging, there is a significant loss of some postmitotic cells, for example, cardiac and skeletal myocytes. Mitochondrial damage and dysfunction with age may trigger increased apoptosis, and this may explain this increase in cell loss. However, it is still unknown if apoptosis plays an important role in normal aging. In vitro it has been shown that several mitochondrial proteins can influence apoptosis, depending on factors such as the mitochondrial membrane potential and cellular redox status. It remains possible that mitochondrial dysfunction due to chronic oxidative stress with age is a cause of apoptosis in vivo . This cell loss may be due to mitochondrial‐triggered apoptosis caused by age‐associated increases in oxidant production or increased activation of mitochondrial permeability transition pores. Results from our laboratory and others are reviewed that relate to apoptosis in the normal aging of the brain cortex, heart, and skeletal muscle. Particular attention is paid to the role of cytochrome c release from mitochondria and alterations in the pro‐ and anti‐apoptotic proteins, Bax and Bcl‐2, respectively. Our results demonstrate that a tissue‐specific adaptation of the Bcl‐2/Bax ratio occurs with age and may directly influence the release of cytochrome c .