MitoQ regulates redox-related non-coding RNAs to preserve mitochondrial network integrity in pressure overload heart failure.

MitoQ regulates redox-related non-coding RNAs to preserve mitochondrial network integrity in pressure overload heart failure. Am J Physiol Heart Circ Physiol. 2020 Jan 31;: Authors: Kim S, Song J, Ernst P, Latimer MN, Ha CM, Goh KY, Ma W, Rajasekaran NS, Zhang J, Liu XM, Prabhu S, Qin G, Wende AR, Young ME, Zhou L Abstract Evidence suggests that mitochondrial network integrity is impaired in cardiomyocytes from failing hearts. While oxidative stress has been implicated in heart failure (HF)-associated mitochondrial remodeling, the effect of mitochondrial-targeted antioxidants, such as mitoquinone (MitoQ), on the mitochondrial network in a model of heart failure (HF) (e.g. pressure overload) has not been demonstrated. Furthermore, the mechanism of this regulation is not completely understood with an emerging role for post-transcriptional regulation via long non-coding RNAs (lncRNA). We hypothesize that MitoQ preserves mitochondrial fusion proteins (i.e. Mfn2) through redox-sensitive lncRNAs, leading to improved mitochondrial network integrity in HF. To test the hypothesis, 8-weeks old C57BL/6J mice were subjected to ascending aortic constriction (AAC), which caused substantial left ventricular (LV) chamber remodeling and contractile dysfunction in one week. Transmission electron microscopy and immunostaining revealed defective inter-mitochondrial and mitochondrial-sarcoplasmic reticulum (SR) ultrastructure in AAC mice compared to Sham...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Tags: Am J Physiol Heart Circ Physiol Source Type: research