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Lookup NU author(s): Dr Maria Camacho EncinaORCiD, Laura Booth, Dr Rachael Redgrave, Dr Omowumi Folaranmi, Professor Ioakim SpyridopoulosORCiD, Professor Gavin RichardsonORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Cardiovascular diseases (CVDs), a group of disorders affecting the heart or blood vessels, are the primary cause of death worldwide, with an immense impact on patient quality of life and disability. According to the World Health Organization, CVD takes an estimated 17.9 million lives each year, where more than four out of five CVD deaths are due to heart attacks and strokes. In the decades to come, an increased prevalence of age-related CVD, such as atherosclerosis, coronary artery stenosis, myocardial infarction (MI), valvular heart disease, and heart failure (HF) will contribute to an even greater health and economic burden as the global average life expectancy increases and consequently the world’s population continues to age. Considering this, it is important to focus our research efforts on understanding the fundamental mechanisms underlying CVD. In this review, we focus on cellular senescence and mitochondrial dysfunction, which have long been established to contribute to CVD. We also assess the recent advances in targeting mitochondrial dysfunction including energy starvation and oxidative stress, mitochondria dynamics imbalance, cell apoptosis, mitophagy, and senescence with a focus on therapies that influence both and therefore perhaps represent strategies with the most clinical potential, range, and utility.
Author(s): Camacho-Encina M, Booth LK, Redgrave RE, Folaranmi O, Spyridopoulos I, Richardson DG
Publication type: Article
Publication status: Published
Journal: Cells
Year: 2024
Volume: 13
Issue: 4
Pages: 353
Online publication date: 17/02/2024
Acceptance date: 15/02/2024
Date deposited: 20/02/2024
ISSN (electronic): 2073-4409
Publisher: MDPI
URL: https://doi.org/10.3390/cells13040353
DOI: 10.3390/cells13040353
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