Dysregulated Nox4 ubiquitination contributes to redox imbalance and age- 2 related severity of acute lung injury

Why do we age?  In a previous paper, Dr. Hecker demonstrated that imbalance among reactive species, contributed by NOX4 and antioxidant defenses, is a major factor in aging.  In this paper, Dr. Hecker demonstrated that aged mice develop more severe lung injury than younger mice when given LPS and then ventilated (a double hit model of injury).  This mimics what is observed in the clinic, i.e. older people are at a higher risk of ARDS than younger people after trauma.  Dr. Hecker followed up this in vivo observations with in studies on senescent microvascular cells and showed that they suffered significantly higher injury than young endothelial cells when exposed to LPS.  Furthermore, they demonstrated that NOX4 was upregulated in both old (senescent)  and young endothelial cells but in senescent endothelial cells NOX4 was not ubiquinated and thus continue to produce reactive species.  This findings increase our understanding of why we age.  Furthermore, they point out that we all should eat more antioxidants or take more vitamin C

Sadis Matalon

Click here for full paper  http://ajplung.physiology.org/content/early/2017/01/03/ajplung.00305.2016