ABSTRACT

It has been estimated that ~ 40% of the cardiac muscle is composed of only mitochondria. The heart supplies blood against gravity to brain because it requires a constant supply of glucose, oxygen, and numerous trophic factors for normal function. Hence, cardiovascular MB is extremely important for normal health and well-being. Recently, Anupama et al. (2018) highlighted that metabolic syndromes are characterized by obesity, hypertension, dyslipidemia, and diabetes, whereas cardiometabolic syndrome, represented by cardiovascular, renal, metabolic, prothrombotic, and inflammatory abnormalities, occur due to defects in the MB. Several human diseases of CMB have been identified involving defective mtDNA as we reported in the RhOmgko cells as an experimental model of PD, AD, and aging (Sharma et al. 2004). The RhOmgko cells exhibit mitochondrial oxidative and nitrative stress due to ONOO-generation, down-regulation of ΔΨ, and complex-1, a rate limiting enzyme system involved in oxidative phosphorylation, triggering CB molecular pathogenesis. Although RhOmgko cells become elliptical and de-differentiated, they do not lose their potential to divide because the nuclear DNA remains structurally and functionally intact in these cells. Transfection of RhOmgko cells with complex-1 gene regained neurotigenesis, tubulinogenesis, myelinogenesis, and synaptogenesis as confirmed by multiple fluorochrome comet assay and digital fluorescence confocal microscopic analysis. The CB molecular pathogenesis was significantly diminished in complex-1-transfected RhOmgko cells.