The cardiovascular system is one of the most energy-demanding in the body. The heart only stores enough energy to function for about 10 seconds, depending entirely on the continuous generation of cellular energy to sustain the contractions and relaxations needed to pump blood through the body.1

Mitochondria — the powerhouses of the cell — are essential to this process, producing adenosine triphosphate (ATP), the cell’s primary energy molecule. At the same time, however, free radicals are created as a natural byproduct of energy generation, which can lead to oxidative stress. Key to this process, ubiquinol supports 95% of cellular energy production within the body and provides antioxidant protection against oxidative damage.2

In this blog, we’ll explore how mitochondria drive cardiovascular health, the connection between oxidative stress, mitochondrial function, and heart health, and how ubiquinol helps protect and support the proper function of mitochondria and the cardiovascular system as a whole.

How Mitochondria Drive Energy Production, Cellular Repair, and Homeostasis in the Cardiovascular System

Energy production takes place in the mitochondria, where electrons harvested from food are transferred through the electron transport chain (ETC). This process allows for the creation of ATP, which supplies the energy necessary for various cellular processes.

Mitochondrial Fission

Mitochondria also play a role in homeostasis. They manage fission and fusion, the division of a single mitochondrion into two and the merging of two or more mitochondria into one. Fission and fusion occur continuously within the cell to help keep the mitochondria and the cell in good health. Fission allows mitochondria to isolate and remove damaged mitochondrial segments for recycling. Fusion enables mitochondria to share contents, such as DNA and proteins, which helps to sustain cellular function and reduce damage.3,4

Through crosstalk with the cell nucleus, mitochondria help manage inflammatory responses. For example, when oxidative damage occurs, mitochondria signal the activation of repair mechanisms in heart cells and inner blood vessel cells (called endothelial cells). When cells are beyond repair, mitochondria regulate apoptosis, or programmed cell death, to prevent the build-up of damaged or dysfunctional cells that may contribute to age-related decline and common health conditions associated with aging.5,6

Mitochondria also manage cell senescence, a state where cells cease to divide but remain metabolically active. Senescence halts the division of impaired cells, limiting the spread of damage. Left unchecked, senescent cells can drive inflammation, underscoring the role of mitochondria in maintaining healthy cellular function.7

The Relationship Between Oxidative Stress, Mitochondrial Function, and Heart Health

As cellular energy is generated, some electrons slip free of the ETC and react with oxygen, becoming reactive oxygen species (ROS). These unstable molecules seek to stabilize themselves by scavenging electrons from any source of electrons, such as cell membranes, proteins, and even DNA. Antioxidants in the body neutralize ROS by donating an electron, which protects important cellular components from free radical damage.

However, when ROS production overwhelms the body’s antioxidant defenses, the body enters a state of oxidative stress. Modern lifestyle factors such as poor diet, insufficient sleep, and exposure to pollutants all contribute to this imbalance, as does the natural decline in antioxidant capacity that comes with aging. If left unchecked, the damage caused by prolonged or severe oxidative stress can build up, harming both the mitochondria and the cell.

Oxidative damage to mitochondria can weaken the ETC, causing the release of more free radicals, further affecting mitochondrial function. This damage hinders the mitochondria’s ability to produce cellular energy, initiate cellular repair mechanisms, and regulate immune responses, which can ultimately impact cardiovascular health. Over time, key impacts may include:

  • Reduced cellular energy production: When mitochondria produce less ATP, this leaves heart cells with
    diminished energy reserves.8
  • LDL oxidation: Excess ROS oxidize low-density lipoprotein (LDL) cholesterol. While oxidation is a normal
    process, too much oxidized LDL in the blood can lead to the formation of sticky LDL molecules that encroach into
    the endothelial cell wall and impact vessel function.8
  • Changes to endothelial function: Oxidative damage can reduce the availability of nitric oxide (NO) in endothelial
    cells and cause chemical and structural changes within the blood vessels that can influence vascular tone and
    elasticity, affecting critical processes like vasodilation.9-11
  • Turning on inflammatory genes: Prolonged oxidative stress upregulates inflammatory genes, triggering
    “inflammaging.”8

Promoting Cardiovascular Wellness With Ubiquinol

Antioxidant

Ubiquinol, the active antioxidant form of coenzyme Q10 (CoQ10), is a lipid-soluble molecule naturally produced within the body that promotes mitochondrial function and plays a multifaceted role in supporting cardiovascular health. It supports cellular energy generation in the ETC, where it acts as an electron carrier, facilitating the flow of electrons and contributing to ATP production. Through its antioxidant action, ubiquinol neutralizes ROS, helping reduce oxidative cellular damage.12 Unlike its oxidized counterpart, ubiquinone, ubiquinol does not need to be converted before it can perform its antioxidant functions.

Supporting mitochondrial function:The heart has the highest concentration of ubiquinol of any organ,13 which is essential for meeting its high-energy demands and protecting against oxidative stress. Cardiomyocytes, heart muscle cells, contain more mitochondria than any other organ’s cells, enabling the rapid supply of ATP necessary to pump the heart. However, their high metabolic rate can lead to increased ROS production, which, combined with the cardiomyocytes’ limited capacity for repair and regeneration, may leave them especially vulnerable to oxidative damage.14 Ubiquinol’s lipidsolubility allows it to penetrate the double-lipid barrier of the mitochondria, where its presence plays a dual role, promoting the efficient production of ATP and supporting mitochondrial function by safeguarding against oxidative stress.

Protecting against LDL oxidation and maintaining endothelial function:Ubiquinol is the predominant form of CoQ10 in the blood, comprising 95% of the total plasma CoQ10 (ubiquinol + ubiquinone) in a healthy adult.15,16 Ubiquinol’s lipid solubility allows it to bind to blood lipids, primarily LDL cholesterol, where it plays a key role in protecting against LDL oxidation, a critical process that supports healthy vascular function.17,18

Enhancing NO production:Ubiquinol supports cardiovascular health by enhancing NO production, which promotes vasodilation and helps maintain vascular tone and elasticity. Its antioxidant properties help prevent ROS from disrupting NO synthesis, further promoting healthy vascular function.11,18

Supporting Blood Vessel Health:Ubiquinol supports cardiovascular health by protecting endothelial cells from oxidative stress. Its antioxidant properties neutralize harmful ROS, while its role in energy production aids cellular repair and function, promoting overall circulatory system health.18

Kaneka Ubiquinol®, an Essential Supplement for Supporting Cardiovascular Wellness

After age 40, the body’s ability to convert ubiquinone into ubiquinol declines, which may cause a decrease in ubiquinol blood levels. Over time, oxidative stress increases within the body, and with the decline of natural antioxidant mechanisms, antioxidant supplementation becomes a crucial component in promoting overall wellness along with a healthy lifestyle.

Backed by more than 85 human clinical studies using Kaneka Ubiquinol® and more than 17 years of consumer experience, Kaneka Ubiquinol® stands out for its rigorous scientific backing, patented manufacturing process, superior bioavailability, regulatory compliance, and proven safety profile. This comprehensive approach underscores our commitment to quality, efficacy, and consumer trust. Bioidentical to the body’s natural ubiquinol, Kaneka Ubiquinol® is a superior, trusted product that is unique in the CoQ10 supplement space.

Kaneka Ubiquinol® has been shown to be two times better absorbed than conventional CoQ10.19 This enhanced absorbability becomes increasingly significant with aging and in the presence of oxidative stress.

In a clinical study, healthy adults taking 200 mg of Kaneka Ubiquinol® daily for at least 30 days showed an increase in blood ubiquinol levels of approximately eight times compared to baseline.20 Because a Kaneka Ubiquinol® supplement requires no conversion in the body to perform antioxidant functions, it is immediately available to offer protection at the cellular level.21

Ubiqionol is

Supplementation with Kaneka Ubiquinol® has been shown in clinical trials to replenish plasma ubiquinol levels and support cardiovascular health by:

  • Yielding higher absorption than conventional CoQ10 supplementation22
  • Promoting healthy levels of blood markers associated with cardiovascular health18,23
  • Promoting vascular health by facilitating proper vasodilation, enhancing NO availability, and protecting LDL
    from oxidation18,25

Ubiquinol QH

An Ally in Cardiovascular Wellness

Whether you are a healthcare practitioner dedicated to enhancing cardiovascular outcomes or a supplement manufacturer striving to deliver top-tier cardiovascular products, Kaneka Ubiquinol® offers the scientific edge your clients need. Connect with us to enhance your offerings and set a new standard in cardiovascular wellness.

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1. Li A, Shami GJ, Griffiths L, et al. Giant mitochondria in cardiomyocytes: cellular architecture in health and disease. Basic Res Cardiol. 2023:118:39.
2. Martini FH. Muscle tissue. In: Fundamentals of Anatomy and Physiology. 12th ed. Upper Saddle River, NJ: Prentice Hall, Inc; 2024: 81-2.
3. Adebayo M, Singh S, Singh AP, Dasgupta S. Mitochondrial fusion and fission: The fine-tune balance for cellular homeostasis. FASEB J. 2021;35(6):e21620.
4. Uchikado Y, Ikeda Y, Ohishi M. Current understanding of the pivotal role of mitochondrial dynamics in cardiovascular diseases and senescence. Front Cardiovasc Med. 2022;9:905072.
5. Uchikado Y, Ikeda Y, Ohishi M. Current understanding of the pivotal role of mitochondrial dynamics in cardiovascular diseases and senescence. Front Cardiovasc Med. 2022;9:905072.
6. Patergnani S, Bouhamida E, Leo S, Pinton P, Rimessi A. Mitochondrial oxidative stress and “mito-inflammation”: actors in the diseases. Biomedicines. 2021;9(2):216.
7. Kumari R, Jat P. Mechanisms of cellular senescence: cell cycle arrest and senescence-associated secretory phenotype. Front Cell Dev Biol. 2021;9:645593.
8. Pallotti F, Bergamini C, Lamperti C, Fato R. The roles of coenzyme Q in disease: direct and indirect involvement in cellular functions. Int J Mol Sci. 2021;23(1):128.
9. Chiong M, Cartes-Saavedra B, Norambuena-Soto I, Mondaca-Ruff D, Morales PE, García-Miguel M, Mellado R. Mitochondrial metabolism and the control of vascular smooth muscle cell proliferation. Front Cell Dev Biol. 2014;2:72.
10. Zhu T, Hu Q, Yuan Y, Yao H, Zhang J, Qi J. Mitochondrial dynamics in vascular remodeling and target-organ damage. Front Cardiovasc Med. 2023;10:1067732.
11. Zhao Y, Vanhoutte PM, Leung SW. Vascular nitric oxide: beyond eNOS. J Pharmacol Sci. 2015;129(2):83-94.
12. Martini FH. Muscle tissue. In: Fundamentals of Anatomy and Physiology, Prentice Hall, Inc, Upper Saddle River, New Jersey, 12th ed., 2024: 943-5.
13. Zozina VI, Covantev S, Goroshko OA, et al. Coenzyme Q10 in cardiovascular and metabolic diseases: current state of the problem. Curr Cardiol Rev. 2018;14(3):164.
14. Piquereau J, Caffin F, Novotova M, et al. Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell? Front Physiol. 2013;4:102.
15. Yamashita S, Yamamoto Y. Simultaneous detection of ubiquinol and ubiquinone in human plasma as a marker of oxidative stress. Anal Biochem. 1997 Jul 15;250(1):66-73.
16. Tang PH, Miles MV, DeGrauw A, et al. HPLC analysis of reduced and oxidized coenzyme Q(10) in human plasma. Clin Chem. 2001 Feb;47(2):256-65.
17. Ernster L, Forsmark-Andrée P. Ubiquinol: an endogenous antioxidant in aerobic organisms. J Clin Invest. 1993;71(8 Suppl):S60-5.
18. Sabbatinelli J, Orlando P, Galeazzi R, et al. Ubiquinol ameliorates endothelial dysfunction in subjects with mild-to-moderate dyslipidemia: a randomized clinical trial. Nutrients. 2020;12(4):1098.
19. Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev. 2014 Jan;3(1):13-7.
20. Hosoe K, Kitano M, Kishida H, et al. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007;47(1):19-28.
21. Kubo H, Yamamoto Y, Fujisawa A. Orally ingested ubiquinol-10 or ubiquinone-10 reaches the intestinal tract and is absorbed by the small intestine of mice mostly in its original form. J Clin Biochem Nutr. 2023 Mar;72(2):101-106.
22. Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clinical Pharmacol Drug Dev. 2014;3(1):13-7.
23. Onur S, Niklowitz P, Jacobs G, et al. Ubiquinol reduces gamma glutamyl transferase as a marker of oxidative stress in humans. BMC Res Notes. 2014 Jul 4;7:427.
24. Kawashima C, Matsuzawa Y, Konishi M, et al. Ubiquinol improves endothelial function in patients with heart failure with reduced ejection fraction: a single-center, randomized double-blind placebo-controlled crossover pilot study. Am J Cardiovasc Drugs. 2020;Aug;20(4):363-72.
25. Zlatohlavek L, Vrablik M, Grauova B, et al. The effect of coenzyme Q10 in statin myopathy. Neuro Endocrinol Lett. 2012;33 Suppl 2:98-101.

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