Ageing and longevity genes in cardiovascular diseases

Abstract

Over the last century, Western societies experienced a demographic shift driven by increased lifespan and decreased fertility, resulting in the subversion of the world's demographic pyramid. In ageing societies, cardiovascular diseases are the major cause of morbidity and mortality, thus representing a major societal and economic burden. Indeed, ageing associates with the deterioration of a genetic network implicated in senescence and longevity, orchestrating deleterious cellular processes that converge in the structural and functional decline of both the myocardium and the vasculature. In this review, we revise a compendium of genes involved in these processes and delineate possible strategies to interfere with them. Dietary interventions (eg intermittent fasting) and sirtuin‐activating compounds are among the most promising interventions shown to promote protective effects on the ageing cardiovascular system. We conclude that ageing and longevity genes modulate cardiovascular function by acting on deleterious downstream processes such as inflammation and oxidative stress, thus representing promising targets for the prevention and treatment of age‐related cardiovascular dysfunction.

TNF‐α antagonism rescues the effect of ageing on stroke: Perspectives for targeting inflamm‐ageing

“…As such, mechanisms involved in ageing hold potential as therapeutic targets for age‐tailored management of ischaemic cerebral events. 25 Over the last years, we and others showed that ageing, vascular dysfunction and age‐dependent cardio‐ and cerebrovascular diseases involve similar pathophysiological processes including the production of reactive oxygen species and the surge of inflammation. 16 , 19 , 20 , 26 , 27 , 28 Indeed, age associates with an augmented chronic smouldering innate immune response, known as inflamm‐ageing, that occurs in the absence of appropriate inflammatory stimuli.…”

Melatonin: A regulator of the interplay between FoxO1, miR96, and miR215 signaling to diminish the growth, survival, and metastasis of murine adenocarcinoma

“…When FoxO activity is compromised throughout the oxidative stress it becomes advantageous for cell survival. For example, knockout of FoxO3a or FoxO1 can reduce ischemia‐induced infarct size in brain to some extent 42 . Ma et al, elucidated that up‐regulated miR‐96‐5p expression would inhibit apoptosis by targeting FoxO1 in hepatocellular carcinoma 43 .…”

Long-term dietary supplementation with plant-derived omega-3 fatty acid improves outcome in experimental ischemic stroke

“…Therefore, our findings might have translational value in the highly susceptible and affected elderly population, which is paradoxically under-represented in clinical trials. Of interest, in both rodents and humans, aging associates to a chronic low-grade activation of the innate immune system in absence of appropriate immunogenic stimuli 51 . Such a dysfunctional process is termed «inflamm-J o u r n a l P r e -p r o o f aging» and thought to play a major role in several age-associated CV diseases including ischemic stroke 52 .…”