Unbalanced p62/SQSTM1 and LC3 countenance in sarcopenic flesh of mice
Sarcopenia is a aging-related detriment of fundamental flesh mass and strength. Preventing sarcopenia is critical for progressing a high peculiarity of life (QOL) in a aged population. However, a molecular resource of sarcopenia has not nonetheless been unraveled and is still a matter of debate.
Determining either a levels of autophagy-related mediators (e.g., p62/SQSTM1, LC3, etc.) in flesh change with ageing is critical to bargain sarcopenia. Such information could raise a healing strategies for attenuating mammalian sarcopenia.
In prior studies, autophagic defects were rescued in a sarcopenic flesh of mice, rats, and humans. However, all these studies concerned usually western blotting analyses of wanton not cell-fractionated flesh homogenates. Thus, these information were deficient to report a adaptive changes in autophagy-linked molecules within sarcopenic muscle.
Associate Professor Kunihiro Sakuma and his colleagues during Toyohashi Tech found a noted accumulation of p62/SQSTM1 in a sarcopenic quadriceps flesh of mice regulating dual opposite methods (western blotting of cell-fractionated homogenates and immunofluorescence). In contrast, a countenance turn of LC3, a partner of p62/SQSTM1 in autophagy progression, was not modulated.
The found autophagic forsake improves a bargain of a resource underlying sarcopenia. The researchers would like to serve investigate this resource with an aim to draw sarcopenia by improving this autophagic forsake regulating nutrient- and pharmaceutical-based treatments.