Key result
Hypertension, obesity, and meta-inflammation drive cardiovascular aging and atherogenesis via mitochondrial and oxidative stress.
Why the study?
Aging is the most significant cardiovascular risk factor and existing geroprotection strategies show limited efficacy, requiring better understanding of shared mechanisms with hypertension and obesity.
Understanding the shared pathophysiological mechanisms among vascular aging, hypertension, obesity, and meta-inflammation could guide the development of novel geroprotective and cardiovascular prevention strategies.
Supports geroprotective strategies targeting meta-inflammation in hypertension and obesity; leaves open validation in prospective interventional trials.
Cardiovascular diseases are the main cause of disability and mortality in the elderly population in developed countries. At the same time, population-based studies have shown that aging remains the most significant risk factor for cardiovascular pathology. Existing geroprotection strategies have not shown high efficiency. At the same time, the mechanisms of the negative impact of known risk factors (such as hypertension, obesity, metabolic disorders) are largely identical to the processes of cardiovascular aging.Pathophysiological processes associated with aging include oxidative stress and mitochondrial dysfunction, impaired autophagy and increased apoptosis, telomere dysfunction, meta-inflammation and fibrosis. They are interconnected and are potentiated by the presence of hypertension and obesity, aggravating cardiovascular aging and provoking atherogenesis.Understanding the key common links in the pathogenesis of these processes will help determine the direction of developing more effective strategies for geroprotection and prevention of cardiovascular pathology.
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Zyubanova et al. (2024) conducted a review in Cardiovascular aging, hypertension, obesity, and meta-inflammation. Hypertension, obesity, and meta-inflammation was evaluated. Hypertension, obesity, and meta-inflammation potentiate pathophysiological processes of cardiovascular aging, including oxidative stress and mitochondrial dysfunction, provoking atherogenesis.
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