Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease
Maria Camacho-Encina1, Laura K Booth2, Rachael E Redgrave1
1Vascular Medicine and Biology Theme, Bioscience Institute, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
Insights
Cardiovascular diseases (CVDs) are a leading cause of death globally. This review explores cellular senescence and mitochondrial dysfunction as key contributors to CVD, highlighting potential therapeutic strategies targeting both.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Mitochondrial Medicine
Background:
- Cardiovascular diseases (CVDs) are the leading global cause of mortality, significantly impacting quality of life.
- Age-related CVDs like atherosclerosis, myocardial infarction (MI), and heart failure (HF) pose a growing health and economic burden due to increasing life expectancy.
- Understanding the fundamental mechanisms of CVD is crucial for developing effective treatments.
Purpose of the Study:
- To review the roles of cellular senescence and mitochondrial dysfunction in the development of cardiovascular diseases.
- To assess recent advancements in targeting mitochondrial dysfunction and cellular senescence for CVD treatment.
- To identify therapeutic strategies that address both cellular senescence and mitochondrial dysfunction for maximum clinical potential.
Main Methods:
- Literature review focusing on cellular senescence and mitochondrial dysfunction in CVD.
- Analysis of recent research on targeting mitochondrial dysfunction (energy metabolism, oxidative stress, dynamics, apoptosis, mitophagy).
- Evaluation of therapeutic strategies influencing both cellular senescence and mitochondrial pathways.
Main Results:
- Cellular senescence and mitochondrial dysfunction are established contributors to cardiovascular disease.
- Recent advances include targeting energy starvation, oxidative stress, mitochondrial dynamics, apoptosis, and mitophagy.
- Therapies that simultaneously target senescence and mitochondrial dysfunction show significant clinical promise.
Conclusions:
- Cellular senescence and mitochondrial dysfunction are critical factors in cardiovascular disease pathogenesis.
- Targeting these pathways, particularly through combined strategies, offers promising avenues for novel CVD therapies.
- Further research into these interconnected mechanisms can lead to more effective clinical interventions for cardiovascular conditions.
Abstract:
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.
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