Coenzyme Q₁₀ (CoQ₁₀)

Coenzyme Q₁₀ (CoQ₁₀), a lipophilic substituted benzoquinone, is a naturally occurring nutrient found within every cell of both animal and plant cells. It is endogenously synthesized and plays a critical role in a variety of cellular processes. CoQ₁₀ is an obligatory component of the respiratory chain in the inner mitochondrial membrane and is also the only endogenous lipid antioxidant, highlighting its singular importance in cellular health and function. Its presence is not limited to the mitochondria but extends to all cellular membranes and is detectable in the blood.

Biochemical Function

CoQ₁₀ is integral to the electron transport chain on the inner membrane of mitochondria, facilitating the conversion of electrons from food into ATP. Its roles, however, extend beyond energy production. It is essential for uncoupling proteins and controls the permeability transition pore in mitochondria. Additionally, CoQ₁₀ is involved in extramitochondrial electron transport and affects membrane physicochemical properties. It impacts gene expression, which can alter overall metabolism. The primary alterations in energetic and antioxidant functions are believed to underpin its therapeutic effects ^[1].

Potential Longevity Benefits

Lifespan

Cellular and Molecular Roles

As the only endogenous lipid antioxidant, CoQ₁₀ is critical in neutralizing free radicals, thus protecting against DNA damage and cellular dysfunction that are symptomatic of aging. By preserving cellular integrity, CoQ₁₀'s antioxidant action is proposed to impede aging and potentially extend cellular lifespan.

It also contributes to the regulation of mitochondrial function, such as influencing uncoupling proteins and the mitochondrial permeability transition pore, which are crucial for cell survival and apoptosis, respectively. Such regulation is particularly important as mitochondrial dysfunction is a noted characteristic of aging ^[1].

Potential Therapeutic Role

CoQ10 has been widely researched for its potential in various health applications, including physical fitness, fertility, antiaging, diabetes management, and heart failure treatment. The therapeutic effects of CoQ10 are attributed to its enhancement of oxidative phosphorylation and its ability to mitigate oxidative stress.

Neurological Diseases

Clinical and experimental studies indicate that CoQ₁₀ supplementation may exert beneficial effects on neurological diseases such as migraine, Parkinson's disease, Huntington's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Friedreich’s ataxia, and multiple sclerosis.^[1]

Hypertension

It is also of interest in the context of central mechanisms controlling blood pressure due to its effects on the brainstem rostral ventrolateral medulla and the hypothalamic paraventricular nucleus, which are related to cardiovascular hypertension.^[1]

Diabetic Retinopathy

A particular area of interest is how CoQ₁₀ might help with a condition called diabetic retinopathy, which is a leading cause of blindness in adults. High blood sugar in diabetes can harm tiny blood vessels in the eye, leading to this condition. The damage causes stress to the eye and can lead to the growth of unhealthy blood vessels, worsening the problem [Citations 55-57]. Since CoQ₁₀ can help the mitochondria work better and has antioxidant properties, it might be useful in treating this eye condition. ^[2]

Phase II clinical trials have been looking at CoQ₁₀ for an early diabetic retinopathy, also called non-proliferative diabetic retinopathy (NPDR). Patients who took 400 mg of CoQ₁₀ every day for 12 weeks to 6 months (different trials) showed improvements in blood flow and energy production in their cells compared to those who didn’t take it. These findings suggest that CoQ₁₀ could help slow down the worsening of this eye disease by improving blood supply and energy use in the eye, which could help prevent the eye damage from getting worse. More studies are needed to see if CoQ₁₀ can help stop diabetic retinopathy from progressing to more severe stages. ^[2]

Dietary Sources and Supplementation

CoQ₁₀ is found naturally in meats, including organ meats such as liver and kidney, fatty fish, and whole grains. Supplementation of CoQ₁₀ has been shown to be safe and well-tolerated, even at high doses, and does not cause serious adverse effects in humans or experimental animals. Newer formulations of CoQ₁₀ and structural derivatives like idebenone and MitoQ are in development to improve absorption and tissue distribution ^[1].

Safety and Side Effects

The safety profile of CoQ₁₀ is notably benign, with it being well-tolerated even at high doses. It does not induce serious adverse effects in either humans or experimental animals. Minor side effects may include stomach upset, loss of appetite, nausea, and headaches. CoQ₁₀'s interaction with various medications, such as blood thinners and chemotherapy drugs, necessitates a consultation with a healthcare professional before beginning supplementation ^[1].

References

↑ ^{Jump up to: 1.0} ^1.1 ^1.2 ^1.3 ^1.4 ^1.5 Rauchová H: Coenzyme Q10 effects in neurological diseases. Physiol Res 2021. (PMID 35199552) [PubMed] [DOI] [Full text] Abstract
Coenzyme Q10 (CoQ10), a lipophilic substituted benzoquinone, is present in animal and plant cells. It is endogenously synthetized in every cell and involved in a variety of cellular processes. CoQ10 is an obligatory component of the respiratory chain in inner mitochondrial membrane. In addition, the presence of CoQ10 in all cellular membranes and in blood. It is the only endogenous lipid antioxidant. Moreover, it is an essential factor for uncoupling protein and controls the permeability transition pore in mitochondria. It also participates in extramitochondrial electron transport and controls membrane physicochemical properties. CoQ10 effects on gene expression might affect the overall metabolism. Primary changes in the energetic and antioxidant functions can explain its remedial effects. CoQ10 supplementation is safe and well-tolerated, even at high doses. CoQ10 does not cause any serious adverse effects in humans or experimental animals. New preparations of CoQ10 that are less hydrophobic and structural derivatives, like idebenone and MitoQ, are being developed to increase absorption and tissue distribution. The review aims to summarize clinical and experimental effects of CoQ10 supplementations in some neurological diseases such as migraine, Parkinson´s disease, Huntington´s disease, Alzheimer´s disease, amyotrophic lateral sclerosis, Friedreich´s ataxia or multiple sclerosis. Cardiovascular hypertension was included because of its central mechanisms controlling blood pressure in the brainstem rostral ventrolateral medulla and hypothalamic paraventricular nucleus. In conclusion, it seems reasonable to recommend CoQ10 as adjunct to conventional therapy in some cases. However, sometimes CoQ10 supplementations are more efficient in animal models of diseases than in human patients (e.g. Parkinson´s disease) or rather vague (e.g. Friedreich´s ataxia or amyotrophic lateral sclerosis).
↑ ^{Jump up to: 2.0} ^2.1 Hill D et al.: Investigational neuroprotective compounds in clinical trials for retinal disease. Expert Opin Investig Drugs 2021. (PMID 33641585) [PubMed] [DOI] Abstract
INTRODUCTION: Retinal neurodegeneration causes irreversible vision loss, impairing quality of life. By targeting neurotoxic conditions, such as oxidative stress and ischemia, neuroprotectants can slow or stop sight loss resulting from eye disease. Despite limimted clinical use of neuroprotectants, there are several promising compounds in early clinical trials (pre-phase III) which may fulfil new therapeutic roles. Search terms relating to neuroprotection and eye disease were used on ClinicalTrials.gov to identify neuroprotective candidates. AREAS COVERED: Research supporting neuroprotection in eye diseases is focused on, ranging from preclinical to phase II, according to the ClinicalTrials.gov database. The compounds discussed are explored in terms of future clinical applications. EXPERT OPINION: The major challenge in neuroprotection research is translation from basic research to the clinic. A number of potential neuroprotectants have progressed to ophthalmology clinical trials in recent years, with defined mechanisms of action - saffron and CoQ10 - targeting mitochondria, and both CNTF and NGF showing anti-apoptotic effects. Enhancements in trial design and patient cohorts in proof-of-concept trials with enriched patient populations and surrogate endpoints should accelerate drug development. A further important consideration is optimising drug delivery to improve individualised management and patient compliance. Progress in these areas means that neuroprotective strategies have a much improved chance of translational success.

[pmid35199552-1] {Jump up to: 1.0} ^1.1 ^1.2 ^1.3 ^1.4 ^1.5 Rauchová H: Coenzyme Q10 effects in neurological diseases. Physiol Res 2021. (PMID 35199552) [PubMed] [DOI] [Full text] Abstract
Coenzyme Q10 (CoQ10), a lipophilic substituted benzoquinone, is present in animal and plant cells. It is endogenously synthetized in every cell and involved in a variety of cellular processes. CoQ10 is an obligatory component of the respiratory chain in inner mitochondrial membrane. In addition, the presence of CoQ10 in all cellular membranes and in blood. It is the only endogenous lipid antioxidant. Moreover, it is an essential factor for uncoupling protein and controls the permeability transition pore in mitochondria. It also participates in extramitochondrial electron transport and controls membrane physicochemical properties. CoQ10 effects on gene expression might affect the overall metabolism. Primary changes in the energetic and antioxidant functions can explain its remedial effects. CoQ10 supplementation is safe and well-tolerated, even at high doses. CoQ10 does not cause any serious adverse effects in humans or experimental animals. New preparations of CoQ10 that are less hydrophobic and structural derivatives, like idebenone and MitoQ, are being developed to increase absorption and tissue distribution. The review aims to summarize clinical and experimental effects of CoQ10 supplementations in some neurological diseases such as migraine, Parkinson´s disease, Huntington´s disease, Alzheimer´s disease, amyotrophic lateral sclerosis, Friedreich´s ataxia or multiple sclerosis. Cardiovascular hypertension was included because of its central mechanisms controlling blood pressure in the brainstem rostral ventrolateral medulla and hypothalamic paraventricular nucleus. In conclusion, it seems reasonable to recommend CoQ10 as adjunct to conventional therapy in some cases. However, sometimes CoQ10 supplementations are more efficient in animal models of diseases than in human patients (e.g. Parkinson´s disease) or rather vague (e.g. Friedreich´s ataxia or amyotrophic lateral sclerosis).

[pmid33641585-2] {Jump up to: 2.0} ^2.1 Hill D et al.: Investigational neuroprotective compounds in clinical trials for retinal disease. Expert Opin Investig Drugs 2021. (PMID 33641585) [PubMed] [DOI] Abstract
INTRODUCTION: Retinal neurodegeneration causes irreversible vision loss, impairing quality of life. By targeting neurotoxic conditions, such as oxidative stress and ischemia, neuroprotectants can slow or stop sight loss resulting from eye disease. Despite limimted clinical use of neuroprotectants, there are several promising compounds in early clinical trials (pre-phase III) which may fulfil new therapeutic roles. Search terms relating to neuroprotection and eye disease were used on ClinicalTrials.gov to identify neuroprotective candidates. AREAS COVERED: Research supporting neuroprotection in eye diseases is focused on, ranging from preclinical to phase II, according to the ClinicalTrials.gov database. The compounds discussed are explored in terms of future clinical applications. EXPERT OPINION: The major challenge in neuroprotection research is translation from basic research to the clinic. A number of potential neuroprotectants have progressed to ophthalmology clinical trials in recent years, with defined mechanisms of action - saffron and CoQ10 - targeting mitochondria, and both CNTF and NGF showing anti-apoptotic effects. Enhancements in trial design and patient cohorts in proof-of-concept trials with enriched patient populations and surrogate endpoints should accelerate drug development. A further important consideration is optimising drug delivery to improve individualised management and patient compliance. Progress in these areas means that neuroprotective strategies have a much improved chance of translational success.

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