Papers

Peer-reviewed International journal
Apr, 2020

Apoptosis inhibition mitigates aging effects in Drosophila melanogaster.

Genetica
  • Hiroaki Kidera
  • ,
  • Toshimitsu Hatabu
  • ,
  • Kazuo H Takahashi

Volume
148
Number
2
First page
69
Last page
76
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1007/s10709-020-00088-1
Publisher
SPRINGER

Aging is a natural biological process that results in progressive loss of cell, tissue, and organ function. One of the causing factors of the aging process is the decrease in muscle mass, which has not been fully verified in Drosophila. Apoptotic cell death may result in aberrant cell loss and can eventually diminish tissue function and muscle atrophy. If so, inhibition of apoptosis may prolong longevity and reduce motor function and muscle mass decline with age in Drosophila flies. Here, we used Drosophila melanogaster as study material, and induced the overexpression of Drosophila inhibitor of apoptosis protein 1 gene to inhibit apoptosis, and investigated the effect of apoptosis inhibition on the longevity and age-related declines in flight and climbing ability and muscle mass. As a result, the inhibition of apoptosis tended to mitigate the aging effects and prolonged longevity and reduced climbing ability decline with age. The current study suggests that apoptosis inhibition could mitigate the aging effects in D. melanogaster. Although such effects have already been known in mammals, the current results suggest that the apoptosis may play a similar role in insects as well.

Link information
DOI
https://doi.org/10.1007/s10709-020-00088-1
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32219590
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000521857100001&DestApp=WOS_CPL
URL
http://link.springer.com/content/pdf/10.1007/s10709-020-00088-1.pdf
URL
http://link.springer.com/article/10.1007/s10709-020-00088-1/fulltext.html
ID information
  • DOI : 10.1007/s10709-020-00088-1
  • ISSN : 0016-6707
  • eISSN : 1573-6857
  • Pubmed ID : 32219590
  • Web of Science ID : WOS:000521857100001

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