tailieunhanh - Báo cáo Y học: The mitochondrial-lysosomal axis theory of aging Accumulation of damaged mitochondria as a result of imperfect autophagocytosis

Cellular manifestations of aging are most pronounced in postmitotic cells, such as neurons and cardiac myocytes. Alterations of these cells, which are responsible for essential functions of brain and heart, are particularly important contributors to the overall aging process. Mitochondria and lysosomes of postmitotic cells suffer the most remarkable age-related alterations of all cellular organelles. Many mitochondria undergo enlargement and structural disorganization, while lysosomes, which are normally responsible for mitochondrial turnover, gradually accumulate an undegradable, polymeric, autofluorescent material called lipofuscin, or age pigment. . | Eur. J. Biochem. 269 1996-2002 2002 FEBS 2002 doi MINIREVIEW The mitochondrial-lysosomal axis theory of aging Accumulation of damaged mitochondria as a result of imperfect autophagocytosis Ulf T. Brunk and Alexei Terman Division of Pathology II Faculty of Health Sciences Linkoping University Sweden Cellular manifestations of aging are most pronounced in postmitotic cells such as neurons and cardiac myocytes. Alterations of these cells which are responsible for essential functions of brain and heart are particularly important contributors to the overall aging process. Mitochondria and lysosomes of postmitotic cells suffer the most remarkable age-related alterations of all cellular organelles. Many mitochondria undergo enlargement and structural disorganization while lysosomes which are normally responsible for mitochondrial turnover gradually accumulate an unde-gradable polymeric autofluorescent material called lipofuscin or age pigment. We believe that these changes occur not only due to continuous oxidative stress causing oxidation of mitochondrial constituents and autophagocytosed material but also because of the inherent inability of cells to completely remove oxidatively damaged structures biological garbage . A possible factor limiting the effectiveness of mitochondial turnover is the enlargement of mitochondria which may reflect their impaired fission. Non-autophago-cytosed mitochondria undergo further oxidative damage resulting in decreasing energy production and increasing generation of reactive oxygen species. Damaged enlarged and functionally disabled mitochondria gradually displace normal ones which cannot replicate indefinitely because of limited cell volume. Although lipofuscin-loaded lysosomes continue to receive newly synthesized lysosomal enzymes the pigment is undegradable. Therefore advanced lipofuscin accumulation may greatly diminish lysosomal degradative capacity by preventing lysosomal enzymes from targeting to

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