{"id":5434,"date":"2016-02-06T02:59:30","date_gmt":"2016-02-06T02:59:30","guid":{"rendered":"http:\/\/www.kurzweilai.net\/?p=273069"},"modified":"2016-02-12T02:31:36","modified_gmt":"2016-02-12T02:31:36","slug":"mitochondria-trigger-cell-aging-researchers-discover","status":"publish","type":"post","link":"https:\/\/hoo.central12.com\/fugic\/2016\/02\/06\/mitochondria-trigger-cell-aging-researchers-discover\/","title":{"rendered":"Mitochondria trigger cell aging, researchers discover"},"content":{"rendered":"<div id=\"attachment_273093\" class=\"wp-caption aligncenter\" style=\"width: 494px;  border: 1px solid #dddddd; background-color: #f3f3f3; padding-top: 4px; margin: 10px; text-align:center; display: block; margin-right: auto; margin-left: auto;\"><img class=\" wp-image-273093\" title=\"mitochondria clearing\" src=\"http:\/\/www.kurzweilai.net\/images\/mitochondria-clearing.jpg\" alt=\"\" width=\"484\" height=\"336\" \/><p style=' padding: 0 4px 5px; margin: 0;'  class=\"wp-caption-text\">Cellular senescence serves as an important anticancer growth-arrest mechanism, but also contributes to aging. This study shows that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in age. (credit: Clara Correia\u2010Melo et al.\/EMBO Journal)<\/p><\/div>\n<p>An international team of scientists led by Jo\u00e3o Passos at Newcastle University has for the first time shown that <a href=\"https:\/\/en.wikipedia.org\/wiki\/Mitochondrion\" >mitochondria<\/a> (the &#8220;batteries&#8221; of the cells) are major triggers for aging, and eliminating them upon the induction of senescence\u00a0prevents senescence in the aging mouse liver.<\/p>\n<p>As we grow old, cells in our bodies accumulate different types of damage and have increased inflammation, factors that are thought to contribute to the aging process.<\/p>\n<p>As described Feb. 4 in an open-access paper in the\u00a0<em>EMBO Journa<\/em>l, the team carried out a series of genetic experiments involving human cells grown in the laboratory and succeeded in eliminating the majority, if not all, the mitochondria from aging cells.<\/p>\n<p><strong>Tricking mitochondria<\/strong><\/p>\n<div id=\"attachment_273096\" class=\"wp-caption aligncenter\" style=\"width: 310px;  border: 1px solid #dddddd; background-color: #f3f3f3; padding-top: 4px; margin: 10px; text-align:center; display: block; margin-right: auto; margin-left: auto;\"><img class=\"size-full wp-image-273096\" title=\"mitochondrion\" src=\"http:\/\/www.kurzweilai.net\/images\/mitochondrion.jpg\" alt=\"\" width=\"300\" height=\"242\" \/><p style=' padding: 0 4px 5px; margin: 0;'  class=\"wp-caption-text\">Components of a typical mitochondrion (credit: Kelvinsong\/Creative Commons)<\/p><\/div>\n<p>Cells can normally eliminate faulty mitochondria by a process called mitophagy. The scientists were able to \u201ctrick\u201d the cells into inducing this process in a grand scale, until all the mitochondria within the cells were physically removed.<\/p>\n<p>To their surprise, they observed that the aging cells, after losing their mitochondria, showed characteristics similar to younger cells &#8212; that is, they became rejuvenated. The levels of inflammatory molecules, oxygen free radicals and expression of genes, which are among the makers of cellular aging, dropped to the level that would be expected in younger cells.<\/p>\n<p>\u201cThis is a very exciting and surprising discovery,&#8221; said\u00a0Passos. &#8220;We already had some clues that mitochondria played a role in the aging of cells, but scientists around the world have struggled to understand exactly how and to what extent these were involved.&#8221;<\/p>\n<p>The team, involving other universities in the UK and the U.S., also deciphered a new mechanism by which mitochondria contribute to aging: mitochondrial biogenesis, the complex process by which mitochondria replicate themselves, is a major driver of cellular aging.<\/p>\n<p>This work was funded by the UK Biotechnology and Biological Sciences Research Council.<\/p>\n<hr \/>\n<p><strong>Abstract of\u00a0<em>Mitochondria are required for pro-ageing features of the senescent phenotype<\/em><\/strong><\/p>\n<p>Cell senescence is an important tumour suppressor mechanism and driver of ageing. Both functions are dependent on the development of the senescent phenotype, which involves an overproduction of pro\u2010inflammatory and pro\u2010oxidant signals. However, the exact mechanisms regulating these phenotypes remain poorly understood. Here, we show the critical role of mitochondria in cellular senescence. In multiple models of senescence, absence of mitochondria reduced a spectrum of senescence effectors and phenotypes while preserving ATP production via enhanced glycolysis. Global transcriptomic analysis by RNA sequencing revealed that a vast number of senescent\u2010associated changes are dependent on mitochondria, particularly the pro\u2010inflammatory phenotype. Mechanistically, we show that the ATM, Akt and mTORC1 phosphorylation cascade integrates signals from the DNA damage response (DDR) towards PGC\u20101\u03b2\u2010dependent mitochondrial biogenesis, contributing to a ROS\u2010mediated activation of the DDR and cell cycle arrest. Finally, we demonstrate that the reduction in mitochondrial content <em>in\u00a0vivo<\/em>, by either mTORC1 inhibition or PGC\u20101\u03b2 deletion, prevents senescence in the ageing mouse liver. Our results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.<\/p>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>An international team of scientists led by Jo&atilde;o Passos at Newcastle University has for the first time shown that mitochondria (the &ldquo;batteries&rdquo; of the cells) are major triggers for aging, and eliminating them upon the induction of senescence&nbsp;prevents senescence in the aging mouse liver. As we grow old, cells in our bodies accumulate different types [&#8230;]<\/p>\n","protected":false},"author":13,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[45,43],"tags":[],"class_list":["post-5434","post","type-post","status-publish","format-standard","hentry","category-biomedlongevity","category-news"],"_links":{"self":[{"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/posts\/5434"}],"collection":[{"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/users\/13"}],"replies":[{"embeddable":true,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/comments?post=5434"}],"version-history":[{"count":3,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/posts\/5434\/revisions"}],"predecessor-version":[{"id":5557,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/posts\/5434\/revisions\/5557"}],"wp:attachment":[{"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/media?parent=5434"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/categories?post=5434"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/hoo.central12.com\/fugic\/wp-json\/wp\/v2\/tags?post=5434"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}