Ablation of Bax and Bak protects skeletal muscle against pressure-induced injury

Bjorn T. Tam, Angus P. Yu, Eric W. Tam, Douglas A. Monks, Xu P. Wang, Xiao M. Pei, Su P. Koh, Thomas K. Sin, Helen K. W. Law, Felix N. Ugwu, Rashmi Supriya, Benjamin Y. Yung, Shea P. Yip, S. C. Wong, Lawrence W. Chan, Christopher W. Lai, Pin Ouyang, Parco M. Siu*

*Corresponding author for this work

    Research output: Contribution to journalJournal articlepeer-review

    8 Citations (Scopus)

    Abstract

    Pressure-induced injury (PI), such as a pressure ulcer, in patients with limited mobility is a healthcare issue worldwide. PI is an injury to skin and its underlying tissue such as skeletal muscle. Muscle compression, composed of mechanical deformation of muscle and external load, leads to localized ischemia and subsequent unloading reperfusion and, hence, a pressure ulcer in bed-bound patients. Although the gross factors involved in PI have been identified, little is known about the exact disease mechanism or its links to apoptosis, autophagy and inflammation. Here, we report that PI is mediated by intrinsic apoptosis and exacerbated by autophagy. Conditional ablation of Bax and Bak activates the Akt-mTOR pathway and Bnip3-mediated mitophagy and preserves mitochondrial contents in compressed muscle. Moreover, we find that the presence/absence of Bax and Bak alters the roles and functions of autophagy in PI. Our results suggest that manipulating apoptosis and autophagy are potential therapeutic targets for treatment and prevention of PI.
    Original languageEnglish
    Article number3689
    JournalScientific Reports
    Volume8
    DOIs
    Publication statusPublished - 27 Feb 2018

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