Ndufc2-flox Mouse

NDUFC2, encoding NADH: ubiquinone oxidoreductase subunit C2, is a subunit of mitochondrial complex I. Mitochondrial complex I is crucial in the oxidative phosphorylation pathway for ATP production, and thus NDUFC2 is important for maintaining normal mitochondrial function and cellular energy metabolism [2,3,4].

In an ischemia-reperfusion injury model, NDUFC2 deficiency decreased antioxidant levels, leading to NLRP3 activation and endothelial mesenchymal transformation (EndoMT) [1]. In a mouse model of complex human disease, Ndufc2 disruption altered complex I assembly and activity, increased reactive oxygen species production and inflammation, and increased stroke susceptibility [3]. In ACS patients, a significant reduction of NDUFC2 expression was detected in circulating mononuclear cells, and in vitro NDUFC2 silencing affected vascular cell viability and angiogenesis while stimulating markers of plaque rupture [4].

In conclusion, NDUFC2 is essential for normal mitochondrial function and energy metabolism. Through gene-knockout or silencing in various models, it has been shown that NDUFC2 deficiency is associated with increased risks of ischemic stroke and acute coronary syndromes, highlighting its potential as a drug target for these diseases [1,3,4].