Analysis reveals oxidative stress impacts NAFLD and CVDs due to obesity, suggesting therapeutic targets for improvement.
Obesity concerns a wide range of the population, tending to become a major factor for diseases progression and fatality rate increase, with its implications concerning the cardiovascular system deterioration. Obesity is closely linked with metabolic derangements concerning the lipid storage and circulation and the cellular metabolism affecting most of the internal organs, especially liver and cellular function. In this current study, an analysis of the linking mechanisms between obesity, lipid deterioration, liver and lipid tissues homeostasis will be performed, with special attention on the pathophysiological characteristics of these detrimental effects on the NAFLD (non-alcoholic fatty liver disease) and the cellular function of the endothelial blood cells, with special reference on the additional burdening of the obesity on the autonomous nervous system signaling and the resulting hypertension. Despite the very complex and pluripotent pathogenic mechanisms with which obesity is intervening in these processes, it could be safely deduced that metabolic and lipid transport manipulation could serve as a crucial factor towards the cellular and tissue function improvement, with the interlinkages in the mechanisms, although highly analyzed, being until nowadays not completely deciphered.
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Varra et al. (2025) studied this question.
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