MedKoo Cat#: 317102 | Name: Mitoquinone mesylate, ethanol solution
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Description:

WARNING: This product is for research use only, not for human or veterinary use.

Mitoquinone mesylate (MitoQ) is a mitochondria-targeted antioxidant derived from ubiquinone (CoQ10) and is conjugated to a lipophilic triphenylphosphonium (TPP) cation to enhance mitochondrial uptake. It functions by scavenging reactive oxygen species (ROS) within mitochondria, thereby reducing oxidative stress and protecting against mitochondrial dysfunction. MitoQ has demonstrated bioactivity in various preclinical and clinical studies, showing potential benefits in neurodegenerative diseases, cardiovascular conditions, and metabolic disorders. For example, in cellular and animal models of Parkinson’s disease, MitoQ has been reported to reduce dopaminergic neuron loss and improve motor function. In cardiovascular research, clinical trials indicate that MitoQ lowers vascular oxidative stress and improves endothelial function in individuals with hypertension. Additionally, MitoQ has been explored in models of hepatic and renal disorders, where it mitigates mitochondrial damage and fibrosis. These effects are supported by dose-dependent reductions in mitochondrial ROS levels, improvements in mitochondrial membrane potential, and decreased markers of inflammation and apoptosis. NOTE: For the convenience of use, this product is supplied as 200mg /mL solution in ethanol-water (1:1, v/v) solution since pure MitoQ10 is a tar-like or waxy semi-solid and very hard to transfer between containers.

Chemical Structure

Mitoquinone mesylate, ethanol solution
Mitoquinone mesylate, ethanol solution
CAS#845959-50-4 (mesylate)

Theoretical Analysis

MedKoo Cat#: 317102

Name: Mitoquinone mesylate, ethanol solution

CAS#: 845959-50-4 (mesylate)

Chemical Formula: C38H47O7PS

Exact Mass: 583.2972

Molecular Weight: 678.82

Elemental Analysis: C, 67.24; H, 6.98; O, 16.50; P, 4.56; S, 4.72

Price and Availability

Size Price Availability Quantity
5mg USD 65.00 Ready to ship
10mg USD 90.00 Ready to ship
25mg USD 150.00 Ready to ship
50mg USD 250.00 Ready to ship
100mg USD 450.00 Ready to ship
500mg USD 1,450.00 Ready to ship
1g USD 2,450.00 Ready to ship
2g USD 4,650.00 Ready to ship
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Related CAS #
845959-50-4 (mesylate) 845959-52-6 (beta-CD complex) 444890-41-9 (cation) 336184-91-9 (bromide)
Synonym
MitoQ; Mito Q10; MitoQ10; MitoQ-10; Mitoubiquinone mesylate; Mitoquinone methanesulfonate; Mitoquinone mesylate; SKQ-1; SKQ 1; SKQ1;
IUPAC/Chemical Name
(10-(4,5-dimethoxy-2-methyl-3,6-dioxocyclohexa-1,4-dien-1-yl)decyl)triphenylphosphonium methanesulfonate
InChi Key
GVZFUVXPTPGOQT-UHFFFAOYSA-M
InChi Code
InChI=1S/C37H44O4P.CH4O3S/c1-29-33(35(39)37(41-3)36(40-2)34(29)38)27-19-8-6-4-5-7-9-20-28-42(30-21-13-10-14-22-30,31-23-15-11-16-24-31)32-25-17-12-18-26-32;1-5(2,3)4/h10-18,21-26H,4-9,19-20,27-28H2,1-3H3;1H3,(H,2,3,4)/q+1;/p-1
SMILES Code
O=C(C(CCCCCCCCCC[P+](C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=CC=C3)=C4C)C(OC)=C(OC)C4=O.CS(=O)([O-])=O
Appearance
Light purple to brown color in ethanol solution (in pure form, MitoQ is a light purple to brown tar-like or waxy semi-solid)
Purity
>98% (or refer to the Certificate of Analysis), supplied as 200 mg/mL in ethanol-water (1:1, v/v)
Shipping Condition
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility
Soluble in DMSO and ethanol.
Shelf Life
>5 years if stored properly
Drug Formulation
This drug may be formulated in DMSO or ethanol.
Stock Solution Storage
0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code
2934.99.9001
More Info
MitoQ is the first molecule specifically designed to decrease mitochondrial oxidative damage to have undergone clinical trials in humans. MitoQ was designed in the late 1990s as a mitochondria-targeted antioxidant by Michael P. Murphy and Robin A. J. Smith. At the time, both were at the University of Otago, Dunedin, New Zealand where Murphy was a mitochondrial biochemist in the Department of Biochemistry and Smith was an organic chemist at the Department of Chemistry. The molecule was made by a PhD student in Smith’s lab, Geoffrey Kelso, and the first publication on MitoQ was in 2001. Since then over 180 publications on MitoQ have been recorded. MitoQ is the first physiologically active form of CoQ10 specifically targeted to mitochondria in order to decrease oxidative damage to have undergone clinical trials in human patients. MitoQ was designed to accumulate extensively within mitochondria in vivo in order to increase the local antioxidant capacity and thereby decrease mitochondrial oxidative damage. To do this MitoQ incorporates a lipophilic cation, that is a positively charged component that is sufficiently hydrophobic, or “oily”, to be able to pass directly through biological membranes. The lipophilic cation used is based on the triphenylphosphonium structure, which is well known to accumulate within the negative mitochondrial matrix. In the solid form of MitoQ the positive charge is neutralised with a negatively charged anion, typically mesylate, to form a salt. MitoQ is present in two different forms, the oxidised ubiquinone form, MitoQuinone and the reduced ubiquinol form, MitoQuinol. MitoQ can refer to either form or to a mixture of the forms. One on the Phase II clinical trials was on Parkinson's disease where patients were given an oral MitoQ dose of 40 or 80 mg per day for a year and compared with placebo. This trial was registered on clinicaltrials.gov as NCT00329056. The Parkinson’s Disease trial did not show a benefit of MitoQ, probably because the irreversible neuronal damage was too great by the time the patients were diagnosed; however, this study did provide a year’s safety data. In the other trial patients with hepatitis C virus who were not responding to antiviral treatments were assessed for prevention of liver inflammation. This trial was registered on clinicaltrials.gov as NCT00433108. The trial in hepatitis C virus patients did show liver protection. These two trials showed that it was safe to target mitochondria in humans long term and other trials for MitoQ are now planned. The development of MitoQ has led to two further developments. One was a skin cream incorporating MitoQ which is used to combat the signs of skin ageing (mitoq.com). The other was an oral supplement containing a low dose of MitoQ which can be used as a nutritional supplement. (from https://en.wikipedia.org/wiki/MitoQ).
Biological target:
Mitochondrially targeted antioxidant that protects against oxidative damage.
In vitro activity:
To demonstrate the effect of MitoQ on oocytes oxidative stress in IVM conditions, the amount of cytoplasmic ROS and GSH were measured (Fig. 1 A, B, C, D). The level of ROS in the 0.01 and 0.02 µM MitoQ supplemented groups significantly decreased (60.11 ± 3.33% and 38.72 ± 1.40%), compared with 0.04 µM MitoQ (70.27 ± 2.16%), in vitro-control (82.63±3.79%) and sham (83.2±4.59%) groups (p<0.05). In contrast, the level of GSH in those groups treated by 0.01 and 0.02 µM MitoQ significantly increased (189.1 ± 6.0 and 231.7 ± 4.28) compared with the 0.04 µM MitoQ, in vitro-control and sham groups (170.18 ± 3.32, 152 ± 2.62 and 151.4 ± 1.70%, respectively (p<0.05)). Assessment of intracellular levels of ROS and GSH in the in vivo-control group showed 33.5 ± 2.5% and 243.5± 1.1%, respectively, which were closed to the 0.02 µM MitoQ supplemented group. The obtained data cleared that the function and quality of IVM oocyte improved after treated by 0.02µM MitoQ. Reference: Iran J Biotechnol. 2020 Jul; 18(3): e2454. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8035425/
In vivo activity:
Synaptic dysfunction is a likely contributing factor causing the cognitive deficits in 3xTg-AD mice. There is a marked increase in synaptic dysfunction with increasing age in these mice coincident with a significant decline of the presynaptic vesicle glycoprotein synaptophysin in their brains (Oddo et al., 2003; McManus et al., 2011). MitoQ treatment of young 3xTg-AD mice inhibits synaptic loss concurrent with MitoQ-mediated inhibition of spatial memory retention deficits (McManus et al., 2011). Our behavioral data with the aged MitoQ-treated animals suggested that this treatment may have a protective effect on synaptic function in aged 3xTg-AD mice, as well. Immunoblotting was used to quantify synaptophysin levels in cortical tissues of 18-month-old female nonTg, 3xTg-AD, and 3xTg-AD mice that had received MitoQ treatments for the preceding five months. The 3xTg-AD mice had much lower levels of synaptophysin than nonTg animals (Fig. 2). MitoQ treatment significantly inhibited synaptophysin loss in these animals, suggesting that preservation of synapses could be behind the improved cognitive performance of the MitoQ-treated mice. Reference: Mol Cell Neurosci. 2019 Dec; 101: 103409. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359863/
Solvent mg/mL mM comments
Solubility
DMSO 50.0 73.66
Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 678.82 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol:
1. Hosseinzadeh Shirzeyli M, Amidi F, Shamsara M, Nazarian H, Eini F, Hosseinzadeh Shirzeyli F, Majidi Zolbin M, Ghaffari Novin M, Daliri Joupari M. Exposing Mouse Oocytes to MitoQ During In Vitro Maturation Improves Maturation and Developmental Competence. Iran J Biotechnol. 2020 Jul 1;18(3):e2454. doi: 10.30498/IJB.2020.154641.2454. PMID: 33850943; PMCID: PMC8035425. 2. Chong L, Li H, Zhu L, Yu G. Regulatory effect of mitoQ on the mtROS-NLRP3 inflammasome pathway in leptin-pretreated BEAS-2 cells. Exp Ther Med. 2021 May;21(5):466. doi: 10.3892/etm.2021.9897. Epub 2021 Mar 8. PMID: 33763153; PMCID: PMC7983181. 3. Young ML, Franklin JL. The mitochondria-targeted antioxidant MitoQ inhibits memory loss, neuropathology, and extends lifespan in aged 3xTg-AD mice. Mol Cell Neurosci. 2019 Dec;101:103409. doi: 10.1016/j.mcn.2019.103409. Epub 2019 Sep 12. PMID: 31521745; PMCID: PMC7359863.
In vitro protocol:
1. Hosseinzadeh Shirzeyli M, Amidi F, Shamsara M, Nazarian H, Eini F, Hosseinzadeh Shirzeyli F, Majidi Zolbin M, Ghaffari Novin M, Daliri Joupari M. Exposing Mouse Oocytes to MitoQ During In Vitro Maturation Improves Maturation and Developmental Competence. Iran J Biotechnol. 2020 Jul 1;18(3):e2454. doi: 10.30498/IJB.2020.154641.2454. PMID: 33850943; PMCID: PMC8035425. 2. Chong L, Li H, Zhu L, Yu G. Regulatory effect of mitoQ on the mtROS-NLRP3 inflammasome pathway in leptin-pretreated BEAS-2 cells. Exp Ther Med. 2021 May;21(5):466. doi: 10.3892/etm.2021.9897. Epub 2021 Mar 8. PMID: 33763153; PMCID: PMC7983181.
In vivo protocol:
1. Young ML, Franklin JL. The mitochondria-targeted antioxidant MitoQ inhibits memory loss, neuropathology, and extends lifespan in aged 3xTg-AD mice. Mol Cell Neurosci. 2019 Dec;101:103409. doi: 10.1016/j.mcn.2019.103409. Epub 2019 Sep 12. PMID: 31521745; PMCID: PMC7359863.
1: Tate AD, Antonelli PJ, Hannabass KR, Dirain CO. Mitochondria-Targeted Antioxidant Mitoquinone Reduces Cisplatin-Induced Ototoxicity in Guinea Pigs. Otolaryngol Head Neck Surg. 2017 Mar;156(3):543-548. doi: 10.1177/0194599816678381. PubMed PMID: 28248600. 2: Pokrzywinski KL, Biel TG, Kryndushkin D, Rao VA. Therapeutic Targeting of the Mitochondria Initiates Excessive Superoxide Production and Mitochondrial Depolarization Causing Decreased mtDNA Integrity. PLoS One. 2016 Dec 28;11(12):e0168283. doi: 10.1371/journal.pone.0168283. PubMed PMID: 28030582; PubMed Central PMCID: PMC5193408. 3: Chu FF, Esworthy RS, Doroshow JH, Grasberger H, Donko A, Leto TL, Gao Q, Shen B. Deficiency in Duox2 activity alleviates ileitis in GPx1- and GPx2-knockout mice without affecting apoptosis incidence in the crypt epithelium. Redox Biol. 2017 Apr;11:144-156. doi: 10.1016/j.redox.2016.11.001. PubMed PMID: 27930931; PubMed Central PMCID: PMC5148781. 4: Escribano-Lopez I, Diaz-Morales N, Rovira-Llopis S, de Marañon AM, Orden S, Alvarez A, Bañuls C, Rocha M, Murphy MP, Hernandez-Mijares A, Victor VM. The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated from type 2 diabetic patients. Redox Biol. 2016 Dec;10:200-205. doi: 10.1016/j.redox.2016.10.017. PubMed PMID: 27810734; PubMed Central PMCID: PMC5094376. 5: Sakellariou GK, Pearson T, Lightfoot AP, Nye GA, Wells N, Giakoumaki II, Griffiths RD, McArdle A, Jackson MJ. Long-term administration of the mitochondria-targeted antioxidant mitoquinone mesylate fails to attenuate age-related oxidative damage or rescue the loss of muscle mass and function associated with aging of skeletal muscle. FASEB J. 2016 Nov;30(11):3771-3785. Epub 2016 Aug 22. PubMed PMID: 27550965; PubMed Central PMCID: PMC5067250. 6: Ham PB 3rd, Raju R. Mitochondrial function in hypoxic ischemic injury and influence of aging. Prog Neurobiol. 2016 Jun 16. pii: S0301-0082(15)30065-4. doi: 10.1016/j.pneurobio.2016.06.006. [Epub ahead of print] Review. PubMed PMID: 27321753; PubMed Central PMCID: PMC5161736. 7: Liu L, Wang MJ, Yu TH, Cheng Z, Li M, Guo QW. [Mitochondria-targeted antioxidant Mitoquinone protects post-thaw human sperm against oxidative stress injury]. Zhonghua Nan Ke Xue. 2016 Mar;22(3):205-11. Chinese. PubMed PMID: 27172658. 8: Lozano-Sepulveda SA, Bryan-Marrugo OL, Cordova-Fletes C, Gutierrez-Ruiz MC, Rivas-Estilla AM. Oxidative stress modulation in hepatitis C virus infected cells. World J Hepatol. 2015 Dec 18;7(29):2880-9. doi: 10.4254/wjh.v7.i29.2880. Review. PubMed PMID: 26692473; PubMed Central PMCID: PMC4678374. 9: Maiti AK, Sharba S, Navabi N, Forsman H, Fernandez HR, Lindén SK. IL-4 Protects the Mitochondria Against TNFα and IFNγ Induced Insult During Clearance of Infection with Citrobacter rodentium and Escherichia coli. Sci Rep. 2015 Oct 20;5:15434. doi: 10.1038/srep15434. PubMed PMID: 26481427; PubMed Central PMCID: PMC4613366. 10: Dare AJ, Logan A, Prime TA, Rogatti S, Goddard M, Bolton EM, Bradley JA, Pettigrew GJ, Murphy MP, Saeb-Parsy K. The mitochondria-targeted anti-oxidant MitoQ decreases ischemia-reperfusion injury in a murine syngeneic heart transplant model. J Heart Lung Transplant. 2015 Nov;34(11):1471-80. doi: 10.1016/j.healun.2015.05.007. PubMed PMID: 26140808; PubMed Central PMCID: PMC4626443. 11: Li Y, Yang J, Chen MH, Wang Q, Qin MJ, Zhang T, Chen XQ, Liu BL, Wen XD. Ilexgenin A inhibits endoplasmic reticulum stress and ameliorates endothelial dysfunction via suppression of TXNIP/NLRP3 inflammasome activation in an AMPK dependent manner. Pharmacol Res. 2015 Sep;99:101-15. doi: 10.1016/j.phrs.2015.05.012. PubMed PMID: 26054569. 12: Huang W, Cash N, Wen L, Szatmary P, Mukherjee R, Armstrong J, Chvanov M, Tepikin AV, Murphy MP, Sutton R, Criddle DN. Effects of the mitochondria-targeted antioxidant mitoquinone in murine acute pancreatitis. Mediators Inflamm. 2015;2015:901780. doi: 10.1155/2015/901780. PubMed PMID: 25878403; PubMed Central PMCID: PMC4386569. 13: Galarreta CI, Forbes MS, Thornhill BA, Antignac C, Gubler MC, Nevo N, Murphy MP, Chevalier RL. The swan-neck lesion: proximal tubular adaptation to oxidative stress in nephropathic cystinosis. Am J Physiol Renal Physiol. 2015 May 15;308(10):F1155-66. doi: 10.1152/ajprenal.00591.2014. PubMed PMID: 25694483. 14: Chen S, Huang J, Zeng Q, Jia Y, Wang J. [Effect of autophagy and mitochondrial coenzyme Q on exocrine function of pancreas in rats with acute sepsis]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2015 Feb;27(2):86-91. doi: 10.3760/cma.j.issn.2095-4352.2015.02.002. Chinese. PubMed PMID: 25665604. 15: Ng MR, Antonelli PJ, Joseph J, Dirain CO. Assessment of mitochondrial membrane potential in HEI-OC1 and LLC-PK1 cells treated with gentamicin and mitoquinone. Otolaryngol Head Neck Surg. 2015 Apr;152(4):729-33. doi: 10.1177/0194599814564934. PubMed PMID: 25550222. 16: Ramsey H, Wu MX. Mitochondrial anti-oxidant protects IEX-1 deficient mice from organ damage during endotoxemia. Int Immunopharmacol. 2014 Dec;23(2):658-63. PubMed PMID: 25466275; PubMed Central PMCID: PMC4394602. 17: Fink BD, Herlein JA, Guo DF, Kulkarni C, Weidemann BJ, Yu L, Grobe JL, Rahmouni K, Kerns RJ, Sivitz WI. A mitochondrial-targeted coenzyme q analog prevents weight gain and ameliorates hepatic dysfunction in high-fat-fed mice. J Pharmacol Exp Ther. 2014 Dec;351(3):699-708. doi: 10.1124/jpet.114.219329. PubMed PMID: 25301169; PubMed Central PMCID: PMC4244581. 18: Jadidian A, Antonelli PJ, Ojano-Dirain CP. Evaluation of apoptotic markers in HEI-OC1 cells treated with gentamicin with and without the mitochondria-targeted antioxidant mitoquinone. Otol Neurotol. 2015 Mar;36(3):526-30. doi: 10.1097/MAO.0000000000000517. PubMed PMID: 25076226. 19: Ramsey H, Zhang Q, Wu MX. Mitoquinone restores platelet production in irradiation-induced thrombocytopenia. Platelets. 2015;26(5):459-66. doi: 10.3109/09537104.2014.935315. PubMed PMID: 25025394; PubMed Central PMCID: PMC4382457. 20: Dongworth RK, Hall AR, Burke N, Hausenloy DJ. Targeting mitochondria for cardioprotection: examining the benefit for patients. Future Cardiol. 2014 Mar;10(2):255-72. doi: 10.2217/fca.14.6. Review. PubMed PMID: 24762253.
1. Supinski GS, Schroder EA, Wang L, Morris AJ, Callahan LAP. Mitoquinone Mesylate (MitoQ) Prevents Sepsis Induced Diaphragm Dysfunction. J Appl Physiol (1985). 2021 Jul 1. doi: 10.1152/japplphysiol.01053.2020. Epub ahead of print. PMID: 34197233. 2. Shyam R, Ogando DG, Choi M, Liton PB, Bonanno JA. Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy. Invest Ophthalmol Vis Sci. 2021 Sep 2;62(12):15. doi: 10.1167/iovs.62.12.15. PMID: 34533563. 3. Zhang T, Wu P, Budbazar E, Zhu Q, Sun C, Mo J, Peng J, Gospodarev V, Tang J, Shi H, Zhang JH. Mitophagy Reduces Oxidative Stress Via Keap1 (Kelch-Like Epichlorohydrin-Associated Protein 1)/Nrf2 (Nuclear Factor-E2-Related Factor 2)/PHB2 (Prohibitin 2) Pathway After Subarachnoid Hemorrhage in Rats. Stroke. 2019 Apr;50(4):978-988. doi: 10.1161/STROKEAHA.118.021590. Erratum in: Stroke. 2020 Mar;51(3):e57. PMID: 30890112; PMCID: PMC6433519. 4. Gouzos M, Ramezanpour M, Bassiouni A, Psaltis AJ, Wormald PJ, Vreugde S. Antibiotics Affect ROS Production and Fibroblast Migration in an In-vitro Model of Sinonasal Wound Healing. Front Cell Infect Microbiol. 2020 Mar 19;10:110. doi: 10.3389/fcimb.2020.00110. PMID: 32266162; PMCID: PMC7096545. 5. Sun K, Xu L, Jing Y, Han Z, Chen X, Cai C, Zhao P, Zhao X, Yang L, Wei L. Autophagy-deficient Kupffer cells promote tumorigenesis by enhancing mtROS-NF-κB-IL1α/β-dependent inflammation and fibrosis during the preneoplastic stage of hepatocarcinogenesis. Cancer Lett. 2017 Mar 1;388:198-207. doi: 10.1016/j.canlet.2016.12.004. Epub 2016 Dec 20. PMID: 28011320. 6. Zhang T, Xu S, Wu P, Zhou K, Wu L, Xie Z, Xu W, Luo X, Li P, Ocak U, Ocak PE, Travis ZD, Tang J, Shi H, Zhang JH. Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats. Exp Neurol. 2019 Jul;317:1-9. doi: 10.1016/j.expneurol.2019.02.009. Epub 2019 Feb 16. PMID: 30779914. 7. Méndez D, Arauna D, Fuentes F, Araya-Maturana R, Palomo I, Alarcón M, Sebastián D, Zorzano A, Fuentes E. Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. Int J Mol Sci. 2020 Aug 27;21(17):6192. doi: 10.3390/ijms21176192. PMID: 32867213; PMCID: PMC7503844. 8. Zhou H, Wang J, Zhu P, Zhu H, Toan S, Hu S, Ren J, Chen Y. NR4A1 aggravates the cardiac microvascular ischemia reperfusion injury through suppressing FUNDC1-mediated mitophagy and promoting Mff-required mitochondrial fission by CK2α. Basic Res Cardiol. 2018 May 9;113(4):23. doi: 10.1007/s00395-018-0682-1. PMID: 29744594. 9. Lee YJ, Kim GH, Park SI, Lim JH. Down-regulation of the mitochondrial i-AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation. J Cell Mol Med. 2020 Jan;24(1):899-909. doi: 10.1111/jcmm.14799. Epub 2019 Nov 14. PMID: 31725201; PMCID: PMC6933342. 10. Shirzeyli MH, Eini F, Shirzeyli FH, Majd SA, Ghahremani M, Joupari MD, Novin MG. Assessment of Mitochondrial Function and Developmental Potential of Mouse Oocytes after Mitoquinone Supplementation during Vitrification. J Am Assoc Lab Anim Sci. 2021 Jul 1;60(4):388-395. doi: 10.30802/AALAS-JAALAS-20-000123. Epub 2021 May 12. PMID: 33980325. 11. Keck F, Kortchak S, Bakovic A, Roberts B, Agrawal N, Narayanan A. Direct and indirect pro-inflammatory cytokine response resulting from TC-83 infection of glial cells. Virulence. 2018;9(1):1403-1421. doi: 10.1080/21505594.2018.1509668. PMID: 30101649; PMCID: PMC6141141. 12. Cesi G, Walbrecq G, Zimmer A, Kreis S, Haan C. ROS production induced by BRAF inhibitor treatment rewires metabolic processes affecting cell growth of melanoma cells. Mol Cancer. 2017 Jun 8;16(1):102. doi: 10.1186/s12943-017-0667-y. PMID: 28595656; PMCID: PMC5465587. 13. Rao VR, Lautz JD, Kaja S, Foecking EM, Lukács E, Stubbs EB Jr. Mitochondrial-Targeted Antioxidants Attenuate TGF-β2 Signaling in Human Trabecular Meshwork Cells. Invest Ophthalmol Vis Sci. 2019 Aug 1;60(10):3613-3624. doi: 10.1167/iovs.19-27542. PMID: 31433458. 14. Kakimoto PA, Serna JDC, de Miranda Ramos V, Zorzano A, Kowaltowski AJ. Increased glycolysis is an early consequence of palmitate lipotoxicity mediated by redox signaling. Redox Biol. 2021 Sep;45:102026. doi: 10.1016/j.redox.2021.102026. Epub 2021 Jun 1. PMID: 34102573; PMCID: PMC8187254. 15. Matthews AT, Soni H, Robinson-Freeman KE, John TA, Buddington RK, Adebiyi A. Doxorubicin-Induced Fetal Mesangial Cell Death Occurs Independently of TRPC6 Channel Upregulation but Involves Mitochondrial Generation of Reactive Oxygen Species. Int J Mol Sci. 2021 Jul 15;22(14):7589. doi: 10.3390/ijms22147589. PMID: 34299212; PMCID: PMC8305841. 16. Zhang T, Wu P, Budbazar E, Zhu Q, Sun C, Mo J, Peng J, Gospodarev V, Tang J, Shi H, Zhang JH. Mitophagy Reduces Oxidative Stress Via Keap1 (Kelch-Like Epichlorohydrin-Associated Protein 1)/Nrf2 (Nuclear Factor-E2-Related Factor 2)/PHB2 (Prohibitin 2) Pathway After Subarachnoid Hemorrhage in Rats. Stroke. 2019 Apr;50(4):978-988. doi: 10.1161/STROKEAHA.118.021590. Erratum in: Stroke. 2020 Mar;51(3):e57. PMID: 30890112; PMCID: PMC6433519. 17. Wang H, Sun X, Lin MS, Ferrario CM, Van Remmen H, Groban L. G protein-coupled estrogen receptor (GPER) deficiency induces cardiac remodeling through oxidative stress. Transl Res. 2018 Sep;199:39-51. doi: 10.1016/j.trsl.2018.04.005. Epub 2018 Apr 25. PMID: 29758174; PMCID: PMC6151279. 18. Hosseinzadeh Shirzeyli M, Amidi F, Shamsara M, Nazarian H, Eini F, Hosseinzadeh Shirzeyli F, Majidi Zolbin M, Ghaffari Novin M, Daliri Joupari M. Exposing Mouse Oocytes to MitoQ During In Vitro Maturation Improves Maturation and Developmental Competence. Iran J Biotechnol. 2020 Jul 1;18(3):e2454. doi: 10.30498/IJB.2020.154641.2454. PMID: 33850943; PMCID: PMC8035425. 19. Desta YT, Wu M, Bai L, Wu X, Xiong M, Weng X. Mitochondrial-targeted ubiquinone alleviates concanavalin A-induced hepatitis via immune modulation. Int Immunopharmacol. 2020 Jul;84:106518. doi: 10.1016/j.intimp.2020.106518. Epub 2020 May 5. PMID: 32380408. 20. Marek-Iannucci S, Ozdemir AB, Moreira D, Gomez AC, Lane M, Porritt RA, Lee Y, Shimada K, Abe M, Stotland A, Zemmour D, Parker S, Sanchez-Lopez E, Van Eyk J, Gottlieb RA, Fishbein MC, Karin M, Crother TR, Rivas MN, Arditi M. Autophagy-mitophagy induction attenuates cardiovascular inflammation in a murine model of Kawasaki disease vasculitis. JCI Insight. 2021 Sep 22;6(18):e151981. doi: 10.1172/jci.insight.151981. PMID: 34403365; PMCID: PMC8492304.