Difference between revisions of "Postmitotic cells mechanism of aging"

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<h3>Complement  System</h3>
 
<h3>Complement  System</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12794047">PMID: 12794047</a><br /></div>
 
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<h3>TNFa</h3>
 
<h3>TNFa</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11197525">PMID: 11197525</a><br /></div>
 
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<h3>IL1b</h3>
 
<h3>IL1b</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16677101">PMID: 16677101</a><br /></div>
 
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<h3>Lipids  Peroxidation</h3>
 
<h3>Lipids  Peroxidation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/23390587">PMID: 23390587</a><br /></div>
 
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<h3>IL6</h3>
 
<h3>IL6</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16677101">PMID: 16677101</a><br /></div>
 
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<h3>Autophagy</h3>
 
<h3>Autophagy</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/21884931">PMID: 21884931</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/17200947">PMID: 17200947</a><br /></div>
 
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<h3>Gene expression changes</h3>
 
<h3>Gene expression changes</h3>
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<h3>Pro-inflammatory  Cytokines</h3>
 
<h3>Pro-inflammatory  Cytokines</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16677101">PMID: 16677101</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/23589904">PMID: 23589904</a><br /></div>
 
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<h3>Disruption of turnover and  Function of membranes</h3>
 
<h3>Disruption of turnover and  Function of membranes</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19167330">PMID: 19167330</a><br /></div>
 
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<h3>Proteolysis</h3>
 
<h3>Proteolysis</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16214036">PMID: 16214036</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16737690">PMID: 16737690</a><br /></div>
 
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<h3>Lipofuscin</h3>
 
<h3>Lipofuscin</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/10928983">PMID: 10928983</a><br /></div>
 
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<h3>Generalized inflammation</h3>
 
<h3>Generalized inflammation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/20444648">PMID: 20444648</a><br /></div>
 
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<h3>P38</h3>
 
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15870258">PMID: 15870258</a><br /></div>
 
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<h3>Postmitotic and weakly  Proliferating cells</h3>
 
<h3>Postmitotic and weakly  Proliferating cells</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/23390587">PMID: 23390587</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/17453017">PMID: 17453017</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19650712">PMID: 19650712</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16737690">PMID: 16737690</a><br /></div>
 
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<h3>Disruption of  Protein turnover</h3>
 
<h3>Disruption of  Protein turnover</h3>
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<h3>NFkB</h3>
 
<h3>NFkB</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19408108">PMID: 19408108</a><br /></div>
 
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<h3>Gene expression  Changes</h3>
 
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<h3>Gene expression changes (SIRT1, AMPK and etc)</h3>
 
<h3>Gene expression changes (SIRT1, AMPK and etc)</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11718811">PMID: 11718811</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19041753">PMID: 19041753</a><br /></div>
 
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<h3>Protein  Carbonylation</h3>
 
<h3>Protein  Carbonylation</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16796807">PMID: 16796807</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/15775985">PMID: 15775985</a><br /></div>
 
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<h3>Energetics</h3>
 
<h3>Energetics</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11004456">PMID: 11004456</a><br /></div>
 
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<h3>Mutations and  Epimutations of  DNA and  Mitochondrion DNA</h3>
 
<h3>Mutations and  Epimutations of  DNA and  Mitochondrion DNA</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/20544884">PMID: 20544884</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/16737690">PMID: 16737690</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19650712">PMID: 19650712</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/22882466">PMID: 22882466</a><br /></div>
 
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<h3>Dysfunctional  Mitochondria</h3>
 
<h3>Dysfunctional  Mitochondria</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16737690">PMID: 16737690</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/19650712">PMID: 19650712</a><br /></div>
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</div>(.//.)<h1>Postmitotic cells mechanism of aging</h1>
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<p>Most pronounced age-related changes occur in long-lived postmitotic cells, such as neurons, retinal pigment epithelium (RPE), cardiac myocytes, and skeletal muscle fibers. These cells are all highly vulnerable to aging due, of course, to their intensive oxygen metabolism and a consequent extensive ROS production; this is especially true for cardiac myocytes, cortical neurons, and RPE cells. A no-less-important contribution to vulnerability of long-lived postmitotic cells to aging is the fact that these cells are replaced rarely, or not at all, and can thus be as old as the organism itself. In contrast, short-lived postmitotic cells, which are frequently replaced because of division and differentiation of stem cells (e.g., intestinal epithelial cells and peripheral blood cells), do not accumulate substantial amounts of waste during their short lifetimes. However, such short-lived postmitotic cells may alter to some extent with organismal age, possibly reflecting changes in stem and progenitor cells, even though their continuous division considerably decreases their intracellular accumulation of waste products. Recently it was shown that the proliferation potential of stem and progenitor cells decreases with age. Because of this deterioration, the efficiency of biologic waste dilution by cell division also decreases in stem and progenitor cells with age, accompanied by the less-frequent replacement of mature short-lived postmitotic cells.</p>
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<p>The comparatively small number of commanding neuroendocrine cells in the hypothalamus produces tropic hormones. These postmitotic cells regulate the outflow of a number of secondary-order hormones from the pituitary gland, which in turn regulate a range of tertiary-order hormones from peripheral endocrine glands at the bottom of the pyramid. It is conceivable that the age-related loss of a limited number of commanders at the top of this pyramid could lead to an overthrow of the whole organism. </p>
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<p>Aging may thus be assumed to be, to a large extent, a result of the deterioration of long-lived postmitotic cells due to their limited renewal capacity, even if oxidative damage to the components of connective tissues, which normally are recycled by matrix metalloproteinases, also contributes to the aging process. The modification of connective tissue components, making them non-degradable, results from metal-dependent oxidation, or from glycation with secondary Amadori rearrangements into advanced glycation end products (AGEs).</p>
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Revision as of 15:17, 17 June 2015

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Postmitotic cells mechanism of aging

Most pronounced age-related changes occur in long-lived postmitotic cells, such as neurons, retinal pigment epithelium (RPE), cardiac myocytes, and skeletal muscle fibers. These cells are all highly vulnerable to aging due, of course, to their intensive oxygen metabolism and a consequent extensive ROS production; this is especially true for cardiac myocytes, cortical neurons, and RPE cells. A no-less-important contribution to vulnerability of long-lived postmitotic cells to aging is the fact that these cells are replaced rarely, or not at all, and can thus be as old as the organism itself. In contrast, short-lived postmitotic cells, which are frequently replaced because of division and differentiation of stem cells (e.g., intestinal epithelial cells and peripheral blood cells), do not accumulate substantial amounts of waste during their short lifetimes. However, such short-lived postmitotic cells may alter to some extent with organismal age, possibly reflecting changes in stem and progenitor cells, even though their continuous division considerably decreases their intracellular accumulation of waste products. Recently it was shown that the proliferation potential of stem and progenitor cells decreases with age. Because of this deterioration, the efficiency of biologic waste dilution by cell division also decreases in stem and progenitor cells with age, accompanied by the less-frequent replacement of mature short-lived postmitotic cells.

The comparatively small number of commanding neuroendocrine cells in the hypothalamus produces tropic hormones. These postmitotic cells regulate the outflow of a number of secondary-order hormones from the pituitary gland, which in turn regulate a range of tertiary-order hormones from peripheral endocrine glands at the bottom of the pyramid. It is conceivable that the age-related loss of a limited number of commanders at the top of this pyramid could lead to an overthrow of the whole organism.

Aging may thus be assumed to be, to a large extent, a result of the deterioration of long-lived postmitotic cells due to their limited renewal capacity, even if oxidative damage to the components of connective tissues, which normally are recycled by matrix metalloproteinases, also contributes to the aging process. The modification of connective tissue components, making them non-degradable, results from metal-dependent oxidation, or from glycation with secondary Amadori rearrangements into advanced glycation end products (AGEs).