• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo

Signaling from dysfunctional mitochondria induces a distinct type of senescence

judith campisi buck institute cellular senescence nad-ampk-p53 pathway

  • Please log in to reply
No replies to this topic

#1 alc

  • Validating/Suspended
  • 208 posts
  • 102
  • Location:Columbus, OH
  • NO

Posted 11 December 2015 - 11:42 PM


from the article:


"Buck Institute faculty Judith Campisi, PhD, says age researchers need to stop thinking of cellular senescence, now accepted as an important driver of aging, as a single phenotype that stems from genotoxic stress. Research from her lab reveals that cellular senescence, a process whereby cells permanently lose the ability to divide, is also induced by signaling from dysfunctional mitochondria - and that the arrested cells secrete a distinctly different "stew" of biologically active factors in a process unrelated to the damaging free radicals that are created in mitochondria as part of oxygen metabolism. The results are published in Cell Metabolism.
lg.php?bannerid=1642&campaignid=355&zone



"We don't yet know how much this process contributes to natural aging," said Campisi, adding that those studies are currently underway. "But we do think the findings are important in addressing mitochondrial diseases, and those age-related diseases, such as some forms of Parkinson's, which involve mitochondrial dysfunction.""


http://medicalxpress...senescence.html



http://www.cell.com/...4131(15)00578-1




 


  • Informative x 1





Also tagged with one or more of these keywords: judith campisi, buck institute, cellular senescence, nad-ampk-p53 pathway

1 user(s) are reading this topic

0 members, 1 guests, 0 anonymous users