Recent studies identified a level of interaction or interplay between mitochondria and innate immune inflammatory responses. Mitochondrial dysfunction is considered both a trigger and target of uncontrolled inflammatory responses (Gurung, Lukens, & Kanneganti, 2015; Mohanty, Tiwari-Pandey, & Pandey, 2019; Yu et al., 2014). As such, this implicates the potential role of impaired mitochondrial homeostasis in the aggravation of cardiovascular injury secondary to COVID-19 (Darwesh, Jamieson, et al., 2019; Darwesh, Keshavarz-Bahaghighat, Jamieson, & Seubert, 2019; Keshavarz-Bahaghighat, Darwesh, Sosnowski, & Seubert, 2020; Samokhvalov et al., 2018). Inflammatory mediators are well documented to trigger several intracellular cascades that alter mitochondrial metabolism and function. For example, the pro-inflammatory cytokines TNF-α, IL-1β and IL-6, found in the serum from COVID-19 patients, can impede mitochondrial oxidative phosphorylation, inhibit ATP production and mitochondrial ROS production exacerbating injury (Jo, Kim, Shin, & Sasakawa, 2016; Naik & Dixit, 2011). Furthermore, IFN-γ and IL-6 can increase mitochondrial ROS production and directly affect the activity of the electron transport chain, which may cause mitochondrial membrane permeabilization, altered mitochondrial dynamics and cell death (Li et al., 2013).