Database Query Results : Coenzyme Q10, ,

CoQ10, Coenzyme Q10: Click to Expand ⟱
Features:
Coenzyme Q10 (CoQ10), also known as ubiquinone, is a fat-soluble antioxidant and a critical component of the mitochondrial electron transport chain, essential for ATP production. Its potential role in Alzheimer’s disease (AD) and cancer has been increasingly studied, mainly due to its effects on oxidative stress, mitochondrial function, and cellular energy metabolism.

Two types: ubiquinone(standard) vs ubiquinol(more bioavailable)

-high content in beef heart -Acts as an antioxidant, reducing ROS
-Some preclinical studies suggest CoQ10 may reduce Aβ-induced neurotoxicity
-CoQ10 is sometimes used with chemotherapy to reduce cardiotoxicity (especially with doxorubicin).
-Essential for ATP (energy) production.

-CoQ10 levels may drop by 25–40% in people taking statins.
-May support mitochondrial function in neurodegenerative diseases, including Alzheimer’s and Parkinson’s

Coenzyme Q10 exists in three redox states:
Form	         Name	          Abbreviation	    Redox state
Oxidized	Ubiquinone	    CoQ10	     Oxidized
Semiquinone	Ubiquinol radical   CoQ10•–	     Intermediate
Reduced	        Ubiquinol	    CoQ10H₂	     Reduced

Most supplements = ubiquinol (reduced, antioxidant)
BPM31510 = ubiquinone (oxidized) (might raise ROS in cancer cells)

-CoQ10 is fat-soluble, so take it alongside meals that include nutrient-dense fats like coconut oil, butter or tallow in moderation
-initial 200-300mg/day (split during day) down to 100mg after 21 days

BPM31510: Pharmaceutical oxidized CoQ10
BPM31510 = oxidized CoQ10 (ubiquinone) in a specialized lipid formulation.
BPM31510 increases Mitochondrial ROS in cancer cells. That increase is intentional, central to its mechanism, and relatively selective for tumor cells.
BPM31510 Studies report in cancer cells:
↑ mitochondrial ROS
↑ lipid peroxidation
↓ NADPH/NADP⁺ ratio
↓ GSH/GSSG ratio
Activation of oxidative stress pathways
Cell death without classic antioxidant rescue
Importantly: Trolox, NAC, or GSH can partially blunt BPM31510 effects, confirming ROS dependence

Scientific Papers found: Click to Expand⟱
4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas- pase-3).
p27↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.

4763- CoQ10,  Chemo,  doxoR,    Effect of Coenzyme Q10 on Doxorubicin Cytotoxicity in Breast Cancer Cell Cultures
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549
ChemoSen∅, CoQ10 had no effect on the ability of doxorubicin to induce apoptosis or inhibit growth or colony formation in both cell lines tested when CoQ10 was applied over a wide dose range.
antiNeop∅, These results support the hypothesis that CoQ10 does not alter the antineoplastic properties of doxorubicin.
*cardioP↑, hypothesized that dietary supplementation of CoQ10 prior to and during doxorubicin treatment can prevent doxorubicin-induced cardiotoxicity by preventing or slowing the displacement of CoQ10 by doxorubicin metabolites.
Dose↝, A daily dose of 300 mg per day for 11 days has been shown to raise plasma CoQ10 concentrations by 300-400%
selectivity↑, CoQ10 increased the cytotoxic activity of doxorubicin in L-1210 leukemia cells and had no effect in Ehrlich ascites carcinoma cells.3
TumCG∅, CoQ10 does not antagonize the in vitro growth inhibition effect of doxorubicin
TumCG∅, The growth inhibition of doxorubicin alone for BT549 cell line of 53.1% was also not significantly altered by CoQ10 additions
Apoptosis∅, CoQ10 does not diminish apoptotic effect of doxorubicin

4776- CoQ10,    Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy
- vitro+vivo, Ovarian, SKOV3
ROS↑, CoQ0 triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented CoQ0-induced apoptosis, but not autophagy
eff↓, whereas antioxidant NAC N-acetylcysteine prevented CoQ0-induced apoptosis, but not autophagy
AntiCan↑, Furthermore, CoQ0 treatment to SKOV-3 xenografted nude mice reduced tumor incidence and burden
Apoptosis↑, Our findings emphasize that CoQ0 triggered ROS-mediated apoptosis and cytoprotective autophagy.
tumCV↓, CoQ0 inhibits viability and growth of human ovarian carcinoma cells
TumCG↓, CoQ0 suppresses tumor growth in SKOV-3 xenografted nude mice
TumCCA↑, CoQ0 induces G2/M cell-cycle arrest and reduces cell-cycle proteins in SKOV-3 cells
LC3s↑, CoQ0 promotes LC3 accumulation and AVOs formation in SKOV-3 cells
ERS↑, CoQ0 triggers apoptotic death of SKOV-3 cells via mitochondrial and ER-stress signals
Beclin-1↑, CoQ0 increases Beclin-1/Bcl-2 and Bax/Bcl-2, and inhibits HER-2/neu/AKT/mTOR signalling in SKOV-3 cells
Bax:Bcl2↑,
HER2/EBBR2↓,
Akt↓,
mTOR↓,

4775- CoQ10,  Chemo,    Chemotherapy induces an increase in coenzyme Q10 levels in cancer cell lines
- in-vitro, Var, NA
ChemoSen↓, Our findings suggest that coenzyme Q10 increase is implicated in the cellular defense under chemotherapy treatment and may contribute to cell survival.
*antiOx↑, CoQ also functions as an antioxidant which protects the cells both directly by preventing lipid peroxidation
*lipid-P?,

4773- CoQ10,    Coenzyme Q10 inhibits the activation of pancreatic stellate cells through PI3K/AKT/mTOR signaling pathway
- in-vitro, Nor, NA
*other↓, Our finding suggests that CoQ10 inhibits the activation of PSCs by suppressing autophagy through activating the PI3K/AKT/mTOR signaling pathway.
*PI3K↑, PI3K/AKT/mTOR signaling pathway were dose-dependently upregulated with increased CoQ10 concentrations
*Akt↑,
*mTOR↑,
*ROS↓, In this study, CoQ10 significantly reduced the intracellular level of ROS in PSCs.

4772- CoQ10,    The anti-tumor activities of coenzyme Q0 through ROS-mediated autophagic cell death in human triple-negative breast cells
- in-vitro, BC, MDA-MB-468 - in-vitro, BC, MDA-MB-231
TumCP↓, Coenzyme Q0 (CoQ0) inhibits proliferation and colony formation in MDA-MB-468 and 231 cells.
Apoptosis↑, CoQ0 induced apoptosis associated with caspase-3 activation and PARP cleavage
Casp3↑,
cl‑PARP↑,
LC3II↑, CoQ0 induced autophagic cell death is accompanied by LC3-II accumulation and AVO formation
eff↓, Antioxidant NAC prevents CoQ0-induced apoptosis and autophagy.
TumCG↓, CoQ0 (Fig. 1A) suppressed TNBC and Hs578T cell growth, as well as dose-dependently reduced cell growth.
Bax:Bcl2↑, CoQ0 increases Bax/Bcl-2 and Beclin-1/Bcl-2 ratio in both TNBC cell lines
Beclin-1↑,
TumAuto↑, CoQ0 induces autophagy, which ultimately results in cell death TNBC cells
ROS↑, CoQ0 activates intracellular ROS generation in TNBC cells. TNBC cells treated with CoQ0 (5 or 7.5 µM for 0–120 min) showed substantially elevated ROS accumulation

4771- CoQ10,    Coenzyme Q10 Protects Astrocytes from ROS-Induced Damage through Inhibition of Mitochondria-Mediated Cell Death Pathway
- Review, Var, NA
*ROS↓, Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases.

4770- CoQ10,  VitK2,    Cancer cell stiffening via CoQ10 and UBIAD1 regulates ECM signaling and ferroptosis in breast cancer
- in-vitro, BC, MDA-MB-231
other↑, CoQ10 and UBIAD1 increase membrane fluidity leading to increased cell stiffness in BC
*antiOx↑, CoQ10 (or ubiquinone) is a potent lipid-soluble antioxidant enriched not only in mitochondria but also in plasma membranes
Risk↓, Loss of the CoQ10-biosynthetic enzyme UBIAD1 is associated to a worse prognosis in BC patients.
other↑, Deletion of Ubiad1 gene accelerates BC development in mouse models.
TumMeta↓, UBIAD1 expression limits metastasis formation in aggressive BC lines
ECM/TCF↓, CoQ10 and UBIAD1 expression impairs ECM-mediated signaling and AKT2 pathway in BC cells
Akt2↓,
Ferroptosis↑, UBIAD1 and CoQ10 enhance BC sensitivity to ferroptosis inducers via FSP1
eff↑, While CoQ10 treatment alone does not affect MDA-MB-231 cell viability, the co-treatment with RSL3 significantly enhanced cell death

4769- CoQ10,    CoQ10 Is Key for Cellular Energy and Cancer Support
- Review, Var, NA
Risk↓, CoQ10, an essential compound for cellular energy production, is often found at low levels in cancer patients, suggesting a link between CoQ10 deficiency and cancer risk
TumCG↓, Research shows CoQ10 helps fight cancer by slowing tumor growth, preventing new blood vessel formation in tumors and triggering self-destruction of abnormal cells
angioG↓,
TumCD↑,
*toxicity↓, The compound helps regulate immune function and inflammation by supporting mitochondrial health and enhancing T-cell activity, while showing minimal side effects even at high doses
*BioAv↑, Simple steps, like splitting doses and pairing CoQ10 with a meal containing fats, aid in its absorption and effectiveness
MMPs↓, reported ability of CoQ10 to suppress something known as MMPs (matrix metalloproteinases)
Inflam↓, A further aspect focused on the anti-inflammatory effects of CoQ10
chemoP↑, Some individuals received significant help in diminishing tumor markers, while others used CoQ10 to mitigate drug side effects.
cardioP↑, According to the authors, coenzyme Q10 shows evidence of lowering that heart strain.
*ROS↓, Researchers explained that coenzyme Q10 is a compound naturally made in your body, essential for mitochondrial energy production and normal oxidative processes
*toxicity↝, Liver enzyme elevation has been reported after prolonged use of doses of 300 milligrams (mg) daily, but this effect did not escalate into overt liver damage.
Dose?, If you have never taken CoQ10 before, aim for 200 mg to 300 mg daily for the first three weeks. After about 21 days, step down to 100 mg daily

4768- CoQ10,    Role of coenzymes in cancer metabolism
- Review, Var, NA
Risk↓, Deficiency of NADH dehydrogenase ubiquinone 1 subunit (Ndufc2), a subunit of CI, has been found in diabetes, cancer, and stroke
*ROS↓, CoQ10 function as an intracellular antioxidant preventing mitochondrial membrane proteins and phospholipids from free radical-induced oxidative damage
AntiCan↑, CoQ10 supplementation has found beneficial effects in diabetes [137,138], huntington's disease [139], coronary heart disease [140,141], congestive cardiac failure [142], fibromyalgia [143,144], and cancer
TumMeta↓, In addition, they observed that the patients with metastasis had lower CoQ10 levels than those who did not
ROS↑, It has been shown in an in vitro study on C57BL/6 mice that treatment with 100 μM CoQ10 for 72 h. can significantly alleviates pancreatic fibrosis by the ROS-triggered PI3K/AKT/mTOR signaling pathway
TumCG↓, Another in vitro and in vivo study on melanoma cells demonstrated that treatment with CoQ10 inhibit cell growth, induce apoptosis and prevent metastasis through suppression of the Wnt/β-catenin signaling pathway
Apoptosis↑,
TumMeta↓,
Wnt↓,
β-catenin/ZEB1↓,
TumCG↓, CoQ10 significantly lowered the growth of prostate cancer cells without affecting non-cancer prostate cells
selectivity↑,
RadioS↑, human glioblastoma cells with CoQ10 combined with radiation therapy and temozolomide, sensitized cells to radiation-induced DNA damage and potentiates temozolomide cytotoxicity
ChemoSen↑,
H2O2↓, In vitro study suggests that treatment of breast cancer cell lines with CoQ10 significantly decrease intracellular H2O2 content and inhibit MMP-2 activity leading to lower invasion and metastasis
MMP2↓,
cardioP↑, acute reversible depression of myocardial function and a chronic irreversible cardiomyopathy were prevented by different doses of CoQ10
ChemoSen∅, a recent study demonstrated that CoQ10 did not inhibit doxorubicin induced cytotoxicity in breast cancer cell lines [
Dose↝, 59 patients undergoing chemotherapy were enrolled and provided with CoQ10 (30 mg), branch chain amino acids (2500 mg), and carnitine (50 mg) for 21 days.

4767- CoQ10,    Efficacy of Coenzyme Q10 for Improved Tolerability of Cancer Treatments: A Systematic Review
- Review, Var, NA
chemoP↑, results suggested that CoQ10 provides some protection against cardiotoxicity or liver toxicity during cancer treatment.
cardioP↑,
hepatoP↑,
eff↝, Further investigations are necessary to determine whether CoQ10 can improve the tolerability of cancer treatments.

4766- CoQ10,    Activities of Vitamin Q10in Animal Models and a Serious Deficiency in Patients with Cancer
- Review, Var, NA
Risk↓, Twenty-two percent of the patients with breast cancer had levels below 0.5.

4764- CoQ10,  VitE,    Auxiliary effect of trolox on coenzyme Q10 restricts angiogenesis and proliferation of retinoblastoma cells via the ERK/Akt pathway
- in-vitro, RPE, Y79 - in-vitro, Nor, ARPE-19 - in-vivo, NA, NA
tumCV↓, CoQ10, alone and with trolox, reduced Y79 cell viability, induced apoptosis through excess ROS generation, and decreased MMP significantly.
Apoptosis↑,
ROS↑,
MMP↓,
TumCCA↑, Both treatments caused G2/M phase cell arrest.
VEGF↓, The combination of CoQ10 and trolox significantly reduced VEGF-A, ERK, and Akt receptor levels, while CoQ10 alone significantly inhibited ERK and Akt phosphorylation.
ERK↓,
Akt↓,
ChemoSen↑, Several studies thereafter reported a higher therapeutic response rate of CoQ10 when used with other chemotherapeutic agents13, 14 while also improving the tolerability of cancer treatments15,16,17.
chemoP↑,
toxicity↓, CoQ10 + trolox have no adverse effect on ARPE-19 cells
angioG↓, Co-culture of Y79 with human umbilical vein endothelial cells (HUVECs) and the CAM assay results prove that both CoQ10 alone and CoQ10 + trolox are effective in mitigating angiogenic proliferation of cells both in vitro and in vivo

3990- CoQ10,    Serum levels of coenzyme Q10 in patients with Alzheimer's disease
- Study, AD, NA
*other∅, These results suggest that these values are not related with the risk for AD or VD.

4762- CoQ10,    The role of coenzyme Q10 as a preventive and therapeutic agent for the treatment of cancers
- Review, Var, NA
*AntiCan↓, Coenzyme Q10 (CoQ10) is a naturally occurring component that performs an anticancer function by reducing oxidative stress.
*ROS↓,
chemoP↑, As a defensive mechanism against oxidative stress elevation in the antioxidative level including CoQ10 is expected, and an increase in these agents can protect cells and organs from side effects of chemotherapeutic drugs.
TumCCA↑, CoQ10 may induce its antitumor effect through multiple mechanisms, including anti-oxidation, anti-inflammation, cell cycle arrest, promoting apoptosis, reducing cell proliferation, inhibiting angiogenesis, suppression of MMPs, and so on
Apoptosis↑,
TumCP↓,
angioG↓,
MMPs↓,
ChemoSen∅, The review points out that: Some studies show improved tolerance without reduced response (chatAI interpretation)

4761- CoQ10,    Elevated levels of mitochondrial CoQ10 induce ROS-mediated apoptosis in pancreatic cancer
- in-vitro, PC, NA - in-vivo, PC, NA
*ETC↝, Coenzyme Q10 is a critical cofactor in the electron transport chain with complex biological functions that extend beyond mitochondrial respiration.
ROS↑, This study demonstrates that delivery of oxidized Coenzyme Q10 (ubidecarenone) to increase mitochondrial Q-pool is associated with an increase in ROS generation, effectuating anti-cancer effects in a pancreatic cancer model.
*antiOx↑, In addition to its role in ETC function, CoQ10 has phenolic antioxidant activity via its ability to undergo hydrogen abstraction by free radicals6
ROS↑, Paradoxically, CoQ10 also exhibits pro-oxidant activity that occurs either due to a CoQ10 semiquinone reaction5 or due to a reaction with oxygen when CoQ10 is in its oxidized state
OCR↓, Delivery of supraphysiologic levels of ubidecarenone via BPM31510 decreases oxygen consumption rates (OCR) in pancreatic cancer
MMP↓, Ubidecarenone enhances succinate-dependent and glycerol-3-phosphate-dependent ROS generation, mitochondrial membrane depolarization, and regulated cell death
TumCD↑,
TumCG↓, BPM31510 (25 mg/kg, b.i.d) resulted in a significant decrease in tumour growth by day 45 after inoculation compared to saline-treated mice
other↝, NOTE: this is oxidized CoQ10, not the same as CoQ10!!!!!!

4258- CoQ10,    Neuroprotective effects of coenzyme Q10-loaded exosomes obtained from adipose-derived stem cells in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, Exo+CoQ10 significantly improved STZ-induced memory impairment compared to CoQ10 and Exo groups alone.
*BDNF↑, BDNF expression increased in the STZ-induced rats after Exo+ CoQ10, when compared to the CoQ10 and Exo groups.
*cognitive↑, this study, Exo+ COQ10 enhanced cognition and memory deficiency in Alzheimer's disease by boosting BDNF and SOX2 levels in the hippocampus.
*SOX2↑,

4257- CoQ10,    Dietary intake of coenzyme Q10 reduces oxidative stress in patients with acute ischemic stroke: a double-blind, randomized placebo-controlled study
- Trial, Stroke, NA
*MDA↓, Significant reductions in serum MDA and IL-6 levels, alongside increased SOD and BDNF levels, were observed in the CoQ10 group.
*IL6↓,
*SOD↑,
*BDNF↑,
*ROS↓, A 30-day regimen of CoQ10 (600 mg/day) resulted in reduced oxidative stress and inflammation, alongside increased BDNF, suggesting potential neuroprotective benefits for post-stroke rehabilitation.
*Inflam↓,
*neuroP↑,

3997- CoQ10,    Coenzyme Q and Its Role in the Dietary Therapy against Aging
- Review, AD, NA
*AntiAge↑, anti-aging potential of CoQ and its possible use in dietary therapies to alleviate the effects of aging.
*Inflam↓, CoQ Exerts Anti-Inflammatory Effects through Its Antioxidant Activity
*antiOx↑,
*Apoptosis↓, protective role of CoQ10 against apoptosis by inducing the inhibition of cell death independently from its free radical scavenging properties or antioxidant effects
*BioAv↑, It has been reported that intestinal absorption is threefold faster if CoQ10 is administrated with food intake in rats
*other↝, Actually, it has been reported that NQO1 expression increases during the initial steps of Alzheimer’s disease, indicating a higher lipid peroxidation coupled to a higher necessity for CoQ-dependent antioxidant activity
*cognitive↑, In older mice with clear cognitive and psychomotor impairments, short-time (15 days) CoQ-supplementation improved spatial learning
*DNAdam↓, dietary CoQ has also been shown to improve DNA repair systems [213,214] and modulate inflammatory signaling cascade as well as to reduce endoplasmic reticulum stress [214].
*ER Stress↓,

3996- CoQ10,    Coenzyme Q10 decreases TNF-alpha and IL-2 secretion by human peripheral blood mononuclear cells
- in-vitro, Nor, NA
*TNF-α↓, TNFalpha secretion was significantly decreased when the cells were incubated with 0.6 and 1.25 muM of CoQ10.

3995- CoQ10,    Effects of Coenzyme Q10 on TNF-alpha secretion in human and murine monocytic cell lines
- in-vitro, NA, NA
*TNF-α↓, TNF-alpha release was significantly decreased to 72 +/- 32%.
*antiOx↑, In conclusion, CoQ10 has moderate anti-inflammatory effects in two monocytic cell lines which could be mediated by its antioxidant activity.
*Inflam↓,

3994- CoQ10,  Se,    Coenzyme Q10 Supplementation in Aging and Disease
- Review, AD, NA - Review, Park, NA
*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks

3993- CoQ10,    Coenzyme Q10 Decreases Amyloid Pathology and Improves Behavior in a Transgenic Mouse Model of Alzheimer’s Disease
- Review, Park, NA - Review, AD, NA
*neuroP↑, Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human trials of Huntington’s disease and Parkinson’s disease, and reduces plaque burden in Aβ
*Aβ↓,
*ROS↓, We now show that CoQ10 reduces oxidative stress and amyloid pathology and improves behavioral performance in the Tg19959 mouse model of AD
*cognitive↑, Importantly, CoQ10-treated mice showed improved cognitive performance during Morris water maze testing.
*antiOx↑, naturally occurring antioxidant compound CoQ10

3992- CoQ10,    Coenzyme Q10
- Review, AD, NA
*antiOx↑, CoQ10 can potentially increase the production of vital antioxidants, such as superoxide dismutase, an enzyme that effectively mitigates vascular oxidative stress in individuals with hypertension. I
*SOD↑,
*lipid-P↓, CoQ10 lowers lipid peroxidation levels by diminishing pro-oxidative compounds.
*ROS↓,
*other?, CoQ10 can improve blood flow and safeguard blood vessels by preserving nitric oxide

3991- CoQ10,    Evaluation of Coenzyme Q as an Antioxidant Strategy for Alzheimer’s Disease
- in-vivo, AD, NA
*ROS↓, Dietary supplementation with CoQ at a dose of 10 g/kg diet to C65/Bl6 mice for one month significantly suppressed brain protein carbonyl levels, which are markers of oxidative damage
*antiOx↑, Our results suggest that oral CoQ may be a viable antioxidant strategy for neurodegenerative disease.


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Results for Effect on Cancer/Diseased Cells:
Akt↓,3,   Akt2↓,1,   AMPKα↑,1,   angioG↓,3,   AntiCan↑,4,   antiNeop∅,1,   antiOx↓,1,   Apoptosis↑,6,   Apoptosis∅,1,   BAX↑,1,   Bax:Bcl2↑,2,   Bcl-2↓,1,   Beclin-1↑,2,   cardioP↑,3,   Casp3↑,2,   chemoP↑,4,   ChemoSen↓,1,   ChemoSen↑,2,   ChemoSen∅,3,   Cyt‑c↑,1,   Dose?,1,   Dose↝,2,   ECM/TCF↓,1,   eff↓,2,   eff↑,2,   eff↝,1,   ERK↓,1,   ERS↑,1,   Ferroptosis↑,1,   H2O2↓,1,   hepatoP↑,1,   HER2/EBBR2↓,1,   Hif1a↓,1,   Inflam↓,1,   LC3II↑,1,   LC3s↑,1,   LDHA↓,1,   MMP↓,2,   MMP2↓,1,   MMPs↓,2,   mTOR↓,2,   OCR↓,1,   other↑,2,   other↝,1,   P21↑,1,   p27↑,1,   cl‑PARP↑,1,   PDH↑,1,   PI3K↓,1,   PTEN↑,1,   RadioS↑,1,   Risk↓,4,   ROS↑,7,   selectivity↑,2,   survivin↓,1,   toxicity↓,1,   TumAuto↑,1,   TumCCA↑,4,   TumCD↑,2,   TumCG↓,6,   TumCG∅,2,   TumCP↓,2,   tumCV↓,2,   TumMeta↓,3,   VEGF↓,1,   Wnt↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 67

Results for Effect on Normal Cells:
Akt↑,1,   AntiAge↑,2,   AntiCan↓,1,   antiOx↑,9,   Apoptosis↓,1,   Aβ↓,1,   BDNF↑,2,   BioAv↑,2,   BP↓,1,   cardioP↑,2,   cognitive↑,3,   DNAdam↓,1,   Dose↝,1,   eff↑,2,   ER Stress↓,1,   ETC↝,1,   HDL↑,1,   IGF-1↑,1,   IGFBP1↑,1,   IL6↓,2,   Inflam↓,4,   LDL↓,1,   lipid-P?,1,   lipid-P↓,2,   MDA↓,1,   memory↑,1,   mTOR↑,1,   neuroP↑,3,   other?,1,   other↓,1,   other↑,1,   other↝,2,   other∅,2,   PI3K↑,1,   QoL↑,1,   RenoP↑,1,   ROS↓,10,   SOD↑,2,   SOX2↑,1,   TNF-α↓,3,   toxicity↓,1,   toxicity↝,1,  
Total Targets: 42

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