Key result
Oxidative stress and inflammation interact via Nrf-2 and NF-κB crosstalk to drive cardiovascular aging.
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Review highlights how oxidative stress and chronic inflammation drive age-related cardiovascular diseases, indicating critical molecular targets like Nrf-2 and NF-κB.
The global population above 60 years has been growing exponentially in the last decades, which is accompanied by an increase in the prevalence of age-related chronic diseases, highlighting cardiovascular diseases (CVDs), such as hypertension, atherosclerosis, and heart failure. Aging is the main risk factor for these diseases. Such susceptibility to disease is explained, at least in part, by the increase of oxidative stress, in which it damages cellular components such as proteins, DNA, and lipids. In addition, the chronic inflammatory process in aging “inflammaging” also contributes to cell damage, creating a stressful environment which drives to the development of CVDs. Taken together, it is possible to identify the molecular connection between oxidative stress and the inflammatory process, especially by the crosstalk between the transcription factors Nrf-2 and NF- κ B which are mediated by redox signalling and are involved in aging. Therapies that control this process are key targets in the prevention/combat of age-related CVDs. In this review, we show the basics of inflammation and oxidative stress, including the crosstalk between them, and the implications on age-related CVDs.
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Almeida et al. (2020) conducted a review in Age-related cardiovascular diseases (hypertension, atherosclerosis, and heart failure). Inflammation and oxidative stress (Nrf-2 and NF-κB crosstalk) was evaluated on Development of age-related cardiovascular diseases. Oxidative stress and chronic inflammation interact via Nrf-2 and NF-κB redox signaling crosstalk to drive age-related cardiovascular diseases in adults over 60 years.
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