MitoQ (mitoquinone) / Antipodean - LARVOL DELTA

Samm50 Downregulation-Driven Mitochondrial Dysfunction Triggers Ferroptosis and Contributes to Ketamine-Induced Neurotoxicity and Cognitive Impairment. (PubMed, Neuropharmacology) - "In vitro, ferroptosis inhibitors Fer-1 and deferoxamine (DFO) reversed ketamine-induced cell death, Fe2+ overload, LPO, and MMP loss, but Fer-1 failed to restore ATP or Samm50 expression. MitoQ rescued ATP, MMP, and ROS...Collectively, ketamine induces hippocampal neurotoxicity and cognitive impairment via a two-step mechanism: it first downregulates Samm50, leading to primary mitochondrial dysfunction (energy failure and oxidative stress); this mitochondrial impairment then triggers ferroptosis through iron accumulation and suppression of GPX4/SLC7A11. Samm50 downregulation serves as a critical upstream event linking mitochondrial dysfunction to ferroptosis, representing a novel therapeutic target for ketamine-induced neuropsychiatric toxicity."

Journal • Alzheimer's Disease • Cognitive Disorders • Metabolic Disorders • Psychiatry • GPX4 • SLC7A11 • TFRC

Synaptic Mitochondrial Oxidative Stress Contributes to Individual Variability in Age-Related Cognitive Inflexibility in Mice. (PubMed, Aging Cell) - "Consistent with these findings, the mitochondria-targeted antioxidant MitoQ improved attentional set-shifting performance in aged mice without affecting initial learning...Together, these results suggest that synaptic mitochondrial oxidative stress in the mPFC contributes to individual vulnerability to cognitive inflexibility. Targeting synaptic mitochondrial oxidative stress may therefore represent a promising strategy to preserve executive function during aging."

Journal • Preclinical • Cognitive Disorders

Mitochondrial ecosystem restoration in Alzheimer's disease: from mechanisms to multi-target therapeutic strategies. (PubMed, Front Cell Dev Biol) - "Accumulating evidence indicates that strategies ranging from antioxidants (e.g., MitoQ) to mitophagy enhancement (e.g., Spautin-1) and biogenesis activation (e.g., PGC-1α Activator) have demonstrated efficacy in preclinical models...While challenges in blood-brain barrier (BBB) penetration and target specificity persist, the field is shifting from single-target scavenging to combinatorial ecosystem repair. Future success will require precise delivery systems, early biomarkers, and a paradigm shift toward treating the neuron as a metabolic ecosystem, though substantial translational challenges remain."

Journal • Review • Alzheimer's Disease • CNS Disorders • Dementia • Inflammation • Metabolic Disorders

Mitochondrial homeostasis in musculoskeletal diseases: from pathogenic mechanisms to precision therapies. (PubMed, Pharmacol Res) - "These include antioxidants like MitoQ and SkQ1, metabolic modulators such as metformin and NAD⁺ boosters, mitophagy inducers like urolithin A, fission inhibitors including Mdivi-1, senolytic agents, and even mitochondrial transplantation. We conclude by proposing a precision medicine framework that matches specific mitochondrial abnormalities with mechanism-based interventions. Drawing on recent preclinical and clinical evidence, this review positions mitochondrial crosstalk as a promising foundation for developing disease-modifying therapies in musculoskeletal medicine."

Journal • Review • Immunology • Metabolic Disorders • Musculoskeletal Diseases • Osteoarthritis • Osteoporosis • Pain • Rheumatoid Arthritis • Rheumatology • Transplantation

Mitochondria-targeted antioxidants (MitoQ and Mito-TEMPO) versus untargeted antioxidants (SOD and CoQ10) improve post-thaw quality of rooster sperm by mitigating mitochondrial oxidative damage. (PubMed, Theriogenology) - "MitoQ reduces electron leakage in the electron transport chain and prevents release of pro-death factors, while Mito-TEMPO scavenges superoxide radicals and maintains mitochondrial redox balance. These results suggest that specific mitochondrial targeting with MitoQ and Mito-TEMPO is an effective strategy to enhance frozen-thawed rooster sperm quality and improve reproductive performance in poultry breeding programs."

Journal

Azilsartan Ameliorates Diabetic Kidney Disease Through Modulation of Inflammation, Pyroptosis, and Mitochondrial Dysfunction. (PubMed, J Diabetes Res) - "AZL improves renal function and pathology in DKD mice, potentially through both hemodynamic (blood pressure lowering) and nonhemodynamic mechanisms. In vitro evidence indicates that AZL suppresses HG-induced mesangial cell pyroptosis by inhibiting mtROS generation and NLRP3 inflammasome activation."

Journal • Diabetes • Diabetic Nephropathy • Inflammation • Metabolic Disorders • Nephrology • Renal Disease • CASP1 • IL1B • NLRP3

Mitochondria in health and disease: cellular powerhouses, signaling centers, and drivers of dysfunction. (PubMed, Front Cell Dev Biol) - "Examples include targeted antioxidants, such as MitoQ and SkQ1, to selectively neutralize mitochondrial ROS, pharmacological modulators to enhance mitochondrial biogenesis and to restore NAD+ homeostasis via PGC-1α activation, gene-editing technologies, such as mitoTALENs and mtZFNs to selectively eliminate pathogenic mitochondrial DNA mutations, and mitochondrial transplantation as a new technique to replace damaged organelles. Together, these novel approaches highlight the need for research in mitochondrial function to change the therapeutic landscape in the management of mitochondrial dysfunction-associated diseases."

Journal • Review • CNS Disorders • Metabolic Disorders • Oncology • Transplantation

Targeting Mitochondria in MASLD: Comparative Evaluation of MitoQ and SS-31 (Elamipretide) in Aged Female Mice under Nutritional Stress. (PubMed, Physiol Res) - "Mitochondrial dysfunction drives MASLD progression. In aged MASLD mice, MitoQ enhances antioxidant defense, SS-31 preserves integrity, and both improve insulin signaling and reduce fibrosis, supporting mitochondrial therapy for MASLD."

Clinical • IO biomarker • Journal • Preclinical • Cardiovascular • Fibrosis • Hepatology • Immunology • Liver Cancer • Liver Cirrhosis • Metabolic Disorders • Metabolic Dysfunction-Associated Steatotic Liver Disease • Oncology • Solid Tumor • BAX • BCL2 • NLRP3 • NRF1 • SOD2 • TFAM

Effect of MitoQ on Platelet Function and Reactive Oxygen Species Generation in Patients With Sickle Cell Anemia (clinicaltrials.gov) - P=N/A | N=18 | Completed | Sponsor: University of Pittsburgh | Recruiting ➔ Completed

Trial completion • Anemia • Genetic Disorders • Hematological Disorders • Sickle Cell Disease

Mitochondrial Antioxidant Therapy Fails to Improve Obese Asthma Outcomes. (PubMed, Respir Med) - "MitoQ was well tolerated but did not improve airway reactivity, asthma control, or lung function. Targeting oxidative stress in people with obesity and poorly controlled asthma with MitoQ is unlikely to be efficacious for the treatment of asthma."

Journal • Asthma • Genetic Disorders • Immunology • Metabolic Disorders • Obesity • Pulmonary Disease • Respiratory Diseases

MitoQ Has Diverse Effects on H2O2-Induced Oxidative Stress and the NRF2 Signalling Pathway in Aortic Smooth Muscle Cells of Different Origins. (PubMed, Cells) - "Moreover, immortalized cells can be used as a model for investigating oxidative stress responses in AAA-SMC, even though they do not react in exactly the same way. Overall, our findings confirm the cytoprotective potential of MitoQ to limit oxidative stress, particularly in AAA-SMC that is clinically observed in the abdominal aneurysm wall."

Journal • Cardiovascular • KEAP1 • NFE2L2

A Bibliometric and Visualized Analysis of Mitochondrial Research in Diabetic Nephropathy. (PubMed, J Vis Exp) - "Intervention-related and methodology-related topics, including SGLT2 inhibitors, MitoQ, caloric restriction, Mendelian randomization, and metabolomics, were also identified. Overall, mitochondrial research in DN has broadened toward mitochondrial quality control, regulated cell death, multi-omics approaches, and intervention-related topics. These bibliometric patterns indicate topic prominence and citation visibility rather than direct mechanistic or clinical evidence and may help identify directions requiring further validation."

Journal • Diabetes • Diabetic Nephropathy • Nephrology • Renal Disease • NLRP3

Mitochondrial dysfunction in ARDS: unraveling the regulatory networks and therapeutic opportunities. (PubMed, Front Immunol) - "Therapeutically, mitochondria-targeted agents (MitoQ, MOTS-c), modulators of mitochondrial dynamics (baicalein, hydrogen), inhibitors of glycolytic enzymes (PFKFB3, PKM2, PDK4), natural compounds (1-octyl itaconate, shikonin, scutellarin), and mesenchymal stromal cell-mediated mitochondrial transfer have shown promise in preclinical models. This review synthesizes current understanding of the regulatory mechanisms linking mitochondrial dysfunction and metabolic reprogramming in ARDS, discusses cell-type-specific contributions, and highlights emerging therapeutic strategies. Targeting mitochondrial homeostasis and the associated glycolytic shift may offer a transformative approach to ARDS treatment, though challenges related to cell specificity, safety, and clinical translation remain."

Journal • Review • Acute Respiratory Distress Syndrome • Metabolic Disorders • Pulmonary Disease • Respiratory Diseases • GAPDH • HIF1A • NLRP3 • PDK4 • PFKFB3 • PGK1 • PKM • STING

Rewiring the mitochondrial NAD+-CoQ axis using metabolic nanomedicine for acute kidney injury therapy. (PubMed, Mater Today Bio) - "Here, we report carrier-free NAD+/MitoQH2 nanoparticles (NM NPs) with ultrasmall size and ROS-responsive properties. Through renal accumulation and ROS-responsive release, NM NPs showed therapeutic efficacy in hypoxia/reoxygenation- and cisplatin-induced AKI models, as evidenced by reduced ROS accumulation, improved mitochondrial oxidative phosphorylation, enhanced autophagy, and attenuated ferroptosis. This work presents a metabolic nanomedicine strategy based on the co-assembly of bioactive molecules to modulate the mitochondrial NAD+-CoQ axis, providing a promising platform for AKI therapy and potentially other mitochondria-associated diseases."

Journal • Acute Kidney Injury • Metabolic Disorders • Nephrology • Renal Disease

Triclosan induces cardiac malformations via an estrogen receptor-ERK-mitochondrial apoptotic signaling axis in zebrafish embryos. (PubMed, J Hazard Mater) - "The mitochondrial-targeted antioxidant MitoQ significantly alleviated ROS generation, mitochondrial injury, and cardiac defects. Furthermore, molecular docking analysis supported strong binding affinities between TCS and key components of the ER-ERK signaling axis, suggesting potential molecular interactions. Overall, this study identifies a previously unrecognized ER-ERK-mitochondrial apoptotic pathway as a central mechanism driving TCS-induced cardiac developmental toxicity, providing mechanistic insight into the cardiovascular developmental risks posed by environmental endocrine disruptors."

Journal • Cardiovascular • Metabolic Disorders • CASP3 • ER

Mitochondrial-targeted Antioxidant Supplementation for Improving Age-related Vascular Dysfunction in Humans (clinicaltrials.gov) - P2 | N=112 | Completed | Sponsor: University of Colorado, Boulder | Active, not recruiting ➔ Completed | Trial completion date: Dec 2026 ➔ Jul 2026

Trial completion • Trial completion date

Mitochondria-targeted therapeutic strategies in assisted reproduction: challenges and potential solutions. (PubMed, Hum Reprod) - "Mitochondria-targeted therapeutic strategies, including pharmacological approaches such as Coenzyme Q10, mitoquinone, resveratrol, rapamycin, and NAD+ precursors, as well as mitochondrial replacement techniques such as maternal spindle and pronuclear transfer, have shown promise in preclinical models; however, clinical outcomes remain heterogeneous and often inconclusive. Rigorous evaluation of safety, particularly for interventions with pleiotropic effects or heritable consequences, remains essential. A more targeted, developmentally informed and systematically validated approach is needed to advance mitochondria-based therapies toward meaningful improvements in reproductive outcomes."

Journal • Metabolic Disorders

Effects of Nutritional Supplements on Vascular Function: A Narrative Review. (PubMed, J Clin Med) - "This review examines nutritional supplements targeting nitric oxide biology (L-arginine/L-citrulline and citrulline derived from watermelon), polyphenol-rich foods and extracts (cocoa flavan-3-ols and grape polyphenols), mitochondrial redox balance (coenzyme Q10 and the mitochondria-targeted antioxidant MitoQ), endothelial glycocalyx-supporting formulations, olive-derived bioactive compounds, curcumin, and S-allyl cysteine. Overall, current evidence suggests that several nutritional supplements may improve surrogate markers of vascular function; however, evidence demonstrating reductions in major cardiovascular events or cardiovascular mortality remains limited. Future research should prioritize adequately powered randomized controlled trials with longer follow-up, standardized supplement formulations, and clinically meaningful cardiovascular outcomes to more clearly define the role of nutritional supplements in cardiovascular prevention."

Journal • Review • Cardiovascular • Inflammation

The Role of Oxidative Stress in Heart Failure: Mechanisms and Therapeutic Targets. (PubMed, Cureus) - "Accordingly, a group of therapies that increase mitochondrial calcium, such as sodium glucose-linked transporter 2 inhibitors and ranolazine, have been investigated as potential treatments in heart failure. A second group of emerging therapies targets oxidative stress by directly scavenging ROS (MitoQ and SS-31) and has also been studied for use in heart failure. Contemporary research developments propose an alternative approach to targeting oxidative stress by enhancing endogenous antioxidant capacity through the administration of nicotinamide adenine dinucleotide (NAD) precursors, thereby increasing intracellular NAD availability."

Journal • Review • Cardiovascular • Congestive Heart Failure • Heart Failure

MitoQ Ameliorates Diabetic Cardiomyopathy by Inhibiting the mtROS-TXNIP-NLRP3 Pathway. (PubMed, Mediators Inflamm) - "MitoQ attenuates diabetic myocardial injury by inhibiting mtROS accumulation and suppressing TXNIP/NLRP3 inflammasome activation. Targeting the mtROS/TXNIP/NLRP3 signaling pathway may represent a promising therapeutic strategy for DCM."

Journal • Cardiomyopathy • Cardiovascular • Diabetes • Fibrosis • Immunology • IL1B • NLRP3 • TXNIP

Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma. (PubMed, bioRxiv) - "The MitoQC mouse was used to evalute mitophagy in response to endothelin-1, along with immunohistochemical analysis of mitophagy proteins...In retinal ganglion cells, parkin expression and activation was unchanged 24 hours after endothelin-1 administration, but was decreased 72 hours following endothelin-1 administration. Taken together, these results suggest that endothelin-1 impacts mitophagy through parkin-independent mechanisms in retinal ganglion cell bodies, and the ganglion cell bodies and optic nerve appear to have different responses to endothelin-1."

Journal • Preclinical • CNS Disorders • Glaucoma • Ophthalmology • EDN1

Sodium selenite attenuates sepsis-induced cardiac inflammation and oxidative injury by regulating TXN2/TXNIP/NLRP3 signaling and ferroptosis. (PubMed, Front Pharmacol) - "Mitoquinone mesylate (MitoQ), an antioxidant specifically targeted to mitochondria, increased TXN2 expression and decreased mtROS, thioredoxin-interacting protein (TXNIP, a negative regulator of TXN), nucleotide-binding oligomerization domain (NOD)-like receptor protein-3 (NLRP3) inflammasome activation, and ferroptosis. The results suggest that the TXN2-ferroptosis-NLRP3 pathway may represent a therapeutic target for sepsis-induced cardiac injury. In addition, we found that Se supplementation improved cardiac function and relieved mtROS accumulation and ferroptosis in sepsis-associated cardiac injury by regulating TXN2 and TXNIP/NLRP3 expression."

Journal • Cardiomyopathy • Cardiovascular • Immunology • Infectious Disease • Inflammation • Septic Shock • Systemic Inflammatory Response Syndrome • NLRC5 • NLRP3 • TXN2 • TXNIP

Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics. (PubMed, J Biochem Mol Toxicol) - "Notable examples include the mitochondria-targeted antioxidant MitoQ (currently in a Phase 2b trial for UC), ClpP (caseinolytic protease P) activators that reprogram T-cell metabolism, and engineered probiotics that deplete pro-inflammatory succinate. This review synthesizes current evidence on mitochondrial dysfunction in UC, bridging molecular mechanisms, immune-metabolic interactions, and emerging therapeutics to propose a new treatment paradigm centered on mitochondrial restoration."

Journal • Review • Gastroenterology • Gastrointestinal Disorder • Immunology • Inflammation • Inflammatory Bowel Disease • Metabolic Disorders • Stress Ulcer • Ulcerative Colitis

Mitoquinone Prevents Cardiac Dysfunction by Normalizing Mitochondrial ROS and Calcium Handling in Acute Myocardial Infarction. (PubMed, Acta Physiol (Oxf)) - "In cardiomyocytes, it attenuated hypertrophy, preserved shortening, and reduced ([Ca2+]i) transient amplitude. MitoQ prevented contractile dysfunction, suggesting that mitochondrial oxidative stress plays a decisive role in myocardial dysfunction during the acute phase of MI. Targeting antioxidant therapy to the mitochondria represents a promising strategy for preventing post-infarction heart failure and opens new perspectives for the development of more effective interventions in the treatment of cardiovascular diseases."

Journal • Cardiovascular • Congestive Heart Failure • Heart Failure • Myocardial Infarction • CAT

Eight Weeks of MitoQ Supplementation Does Not Alter Kidney Function or Urinary Kidney Injury Biomarkers in Middle-Aged and Older Adults. (PubMed, Am J Physiol Renal Physiol) - "For example, TIMP-2 × IGFBP7 was not different between groups (pre placebo: 114 ± 162, post placebo: 138 ± 161; pre MitoQ: 162 ± 238, post MitoQ: 127 ± 137 ng2/min; interaction p = 0.754). Eight weeks of MitoQ supplementation doesn't appear to benefit or harm kidney function or kidney injury markers in middle-aged and older adults."

Biomarker • Journal • Acute Kidney Injury • Chronic Kidney Disease • Nephrology • Renal Disease • CST3 • IGFBP7 • KIM1 • LCN2 • TIMP2