Adverse Childhood ExperiencePROMISENCT07244809
Probing the Role of Mitochondrial Oxidative Stress in Impaired Vascular Function Among Young Adults With Early Life Adversity
A study testing Mitoquinone mesylate (MitoQ) in people with Adverse Childhood Experience and Endothelial Function (FMD), run by University of Iowa at 1 site in United States.
Trial summary
Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. Greater exposure to ACEs are associated with greater increases in the risk of cardiovascular diseases and death. Read more about this study
- Who is it for?
- Ages 18 to 29 yearsHealthy volunteers can take part
- Conditions the study is for
- Adverse Childhood Experience, Endothelial Function (FMD), Endothelial Injury
- What is being tested?
- Mitoquinone mesylate (MitoQ)
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 300 participants
- Where
- 1 siteUnited States
- Study dates
- 13 Oct 2025to 31 Dec 2026
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 29 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- 18-29 years
- ACE score >=4
Who cannot join
- Resting arterial blood pressure >140/90 mmHg
- BMI <=17 or >= 35
- Are on a weight-loss diet or involved in a formal weight-loss program or are not intentionally weight stable for 6 months (+/- 5 kg) prior to the study.
- Cardiovascular or metabolic prescription drug use
- Vasoactive antidepressant drug use (SSRIs and clonidine)
- Current heavy alcohol use, as defined as binge drinking on 5 or more days in the last month, or consuming more than 7 (women) or 14 (men) drinks per week in the last month (per NIAAA definition)
Show all 12Show fewer
- Current or recent (within the last 6 mo.) illicit drug use disorder as indicated by a score of 3 or greater on the Drug Abuse Screening Test (DAST-10)
- Current tobacco or nicotine use
- Vaping
- Regular vigorous (>6 METs) aerobic exercise (>4 bouts/week, >30 min/bout)
- dietary supplementation with antioxidants or habitual use of NSAIDs
- Currently pregnant or breastfeeding
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
United States1 site, 1 recruiting
- Recruiting
Integrative Laboratory of Applied Physiology and Lifestyle Medicine
Iowa City, Iowa, 52242
Nathaniel Jenkins, PhD, 3194673091, nathaniel-jenkins@uiowa.edu
About this study
Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. Greater exposure to ACEs are associated with greater increases in the risk of cardiovascular diseases and death. Our laboratory has previously observed that vascular function is disrupted in young adults with prior ACE exposure, even though these individuals appear to be healthy clinically (i.e., no classic clinical cardiovascular disease risk factors). There is a need to identify and understand the biological mechanisms underlying these vascular impairments to inform effective interventions to reduce cardiovascular risks the millions of individuals affected by ACEs.
The body's response to stress is coordinated across various systems, all of which depend on energy supplied by mitochondria (often referred to as the "powerhouse of cells"). Based on new evidence across multiple physiological systems from our team, our overarching hypothesis is that disruption of mitochondrial function contributes to cardiovascular impairments among young adults with ACEs. Here we propose the initial pilot work necessary to begin to understand these associations, which will directly inform identification of individuals who may be most vulnerable to stress-related cardiovascular risk and the development of interventions to promote cardiovascular-stress resilience.
Read more
Our aims are to:
- Determine whether mitochondrial oxidative stress contributes to impaired vascular function among young adults who experienced early life adversity.
- Determine whether reducing mitochondrial oxidative stress improves the cellular stress and integrated cardiovascular response to laboratory-based psychosocial stress among young adults who experienced early life adversity.
Read the detailed description
Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. ACEs promote cardiovascular morbidity and mortality in a graded, dose-dependent manner1 and are thus a significant, widespread determinant of cardiovascular disease (CVD). In agreement with preclinical evidence,2 we have established that young adults (18-29 y) with prior ACE exposure exhibit impaired vascular endothelial function (VEF)3 as evidenced by reduced flow mediated dilation even in the absence of clinical CVD risk factors. The vascular endothelium is a regulatory organ that plays a critical role in maintaining cardiovascular homeostasis, and our findings indicate that vascular endothelial dysfunction is one of the earliest identifiable pathophysiological mechanisms linking ACE exposure with future CVD. There remains a critical biomedical need to identify and understand the psychobiological mechanisms underlying ACEs-related vascular endothelial dysfunction to inform effective interventions to improve cardiovascular health in the millions of individuals affected by ACEs. The physiologic response to stress is coordinated across various physiological systems, all of which depend on energy supplied at the cellular level by mitochondria. Based on novel evidence across multiple physiological systems from our team, our overarching hypothesis is that dysregulation of mitochondrial function due to chronic stress burden - or mitochondrial allostatic load (MAL) - promotes dysregulation of the physiological stress response which is ultimately transduced to impairments in VEF in young adults with ACEs. Notably, our preliminary evidence also suggests that psychological resilience and executive functions such as cognitive reappraisal may moderate these relations, reducing MAL and preserving VEF in the face of substantial adversity. Here we propose the critical work necessary to understand these associations, which will directly inform identification of individuals who may be most vulnerable to stress-related cardiovascular risk and the development of interventions to promote cardiovascular-stress resilience.
In this study, we will use an acute dose of a mitochondrial targeted antioxidant supplement (MitoQ; or placebo) to experimentally interrogate the role of mitochondrial oxidative stress is associated with improvements in 1) vascular endothelial function and 2) cellular and integrated cardiovascular responses to a standardized laboratory based psychosocial stressor in young adults with Adverse Childhood Experiences.
Participants will report to the laboratory, provide a blood sample and have vascular endothelial function assessed using a specialized test known as flow mediated dilation, consume a single acute dose of MitoQ previously demonstrated to be effective and safe for acutely decreasing mitochondrial oxidative stress in humans OR placebo, and then have vascular endothelial function measured again. Next, participants will provide another blood sample before undergoing a standardized and commonly used laboratory psychosocial stress test known, before providing additional blood samples after test completion.
- Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The adverse childhood experiences (ace) study. American Journal of Preventive Medicine. 1998;14:245-58. 2. Su S, Jimenez MP, Roberts CT, Loucks EB. The role of adverse childhood experiences in cardiovascular disease risk: A review with emphasis on plausible mechanisms. Curr Cardiol Rep. 2015;17:88. PMC4941633 3. Jenkins NDM, Rogers EM, Banks NF, Tomko PM, Sciarrillo CM, Emerson SR, Taylor A, et al. Childhood psychosocial stress is linked with impaired vascular endothelial function, lower sirt1, and oxidative stress in young adulthood. Am J Physiol Heart Circ Physiol. 2021;321:H532-H41. PMC8461842
- Conditions
- Adverse Childhood Experience, Endothelial Function (FMD), Endothelial Injury, Mitochondrial Function, Oxidative Stress, Psychosocial Influence on Cardiovascular Disease
- Being tested
- Mitoquinone mesylate (MitoQ), Placebo
- Keywords
- flow mediated dilation, mitoquinone mesylate, placebo, early life adversity, trier social stress test
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Mitoquinone mesylate (MitoQ)Dietary supplement
Participants will consume a single 160 mg dose of mitoquinone mesylate, provided in the form of 6, 20 mg capsules, with water.
PlaceboDietary supplement
Participants will consume a single 160 mg dose of microcrystalline cellulose and tapioca (placebo), provided in 20 mg capsules, with water.
| Study group | Role | What they receive |
|---|---|---|
| Mitoquinone Mesylate (MitoQ) | Experimental | Mitoquinone Mesylate (160 mg, single dose) Receives: Dietary Supplement: Mitoquinone mesylate (MitoQ) |
| Placebo | Placebo comparator | Matched placebo (microcrystalline cellulose and tapioca, 160 mg, single dose) Receives: Dietary Supplement: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Vascular endothelial function
Vascular endothelial function will be assessed using the brachial artery flow mediated dilation technique
Measured: Prior to supplementation and 60 minutes after supplementation
Blood pressure
The blood pressure response to psychosocial stress induced by the Trier Social Stress Test will be determined using beat-to-beat blood pressure measurement by finger photoplethysmography (or brachial artery blood pressure in the case of equipment errors). The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
Endothelial Cell Microparticle Release
Endothelial cell microparticle release will be quantified from platelet-poor plasma in response to psychosocial stress induced by the Trier Social Stress Test. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 min following the Trier Social Stress Test.
Cortisol
Cortisol will be quantified from drool collected passively to assess the HPA-axis response to psychosocial stress induced by the Trier Social Stress Test. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 min following the Trier Social Stress Test.
Secondary outcomes (3)
Total Peripheral Resistance
The total peripheral resistance response to psychosocial stress induced by the Trier Social Stress Test will be determined using beat-to-beat blood pressure measurement by finger photoplethysmography. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
Cardiac Output
The cardiac output response to psychosocial stress induced by the Trier Social Stress Test will be determined using beat-to-beat blood pressure measurement by finger photoplethysmography using ModelFlow. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
Growth Differentiation Factor 15
Induction of GDF-15 will be quantified from plasma in response to psychosocial stress induced by the Trier Social Stress Test. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Measured: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 minutes after completion of the Trier Social Stress Test.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 Nov 2025
- Study start13 Oct 2025
- Primary completion31 Jul 2026 (estimated)
- Study completion31 Dec 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Adverse Childhood ExperienceStudies of the same condition, open and under way.
- More trials run by University of IowaThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind
- Who is masked
- Participant, Investigator, Outcomes assessor
- Enrolment
- 300 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Iowa
- Sponsor type
- University, hospital or other
- Collaborators
- MitoQ Limited
- Responsible party
- Principal investigator, Nathaniel Jenkins, University of Iowa
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07244809
- Sponsor's protocol ID
- 202504919
- Acronym
- PROMISE
- Status last verified
- Nov 2025
- First submitted
- 17 Nov 2025
- Last updated
- 24 Nov 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Jenkins NDM, Rogers EM, Banks NF, Tomko PM, Sciarrillo CM, Emerson SR, Taylor A, Teague TK. Childhood psychosocial stress is linked with impaired vascular endothelial function, lower SIRT1, and oxidative stress in young adulthood. Am J Physiol Heart Circ Physiol. 2021 Sep 1;321(3):H532-H541. doi: 10.1152/ajpheart.00123.2021. Epub 2021 Jul 30.
PubMed 34328346Su S, Jimenez MP, Roberts CT, Loucks EB. The role of adverse childhood experiences in cardiovascular disease risk: a review with emphasis on plausible mechanisms. Curr Cardiol Rep. 2015 Oct;17(10):88. doi: 10.1007/s11886-015-0645-1.
PubMed 26289252Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, Marks JS. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998 May;14(4):245-58. doi: 10.1016/s0749-3797(98)00017-8.
PubMed 9635069
Study at a glance
From the registry record, last updated by the sponsor on 24 Nov 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Probing the Role of Mitochondrial Oxidative Stress in Impaired Vascular Function Among Young Adults With Early Life Adversity
- ClinicalTrials.gov ID
- NCT07244809
- Acronym / sponsor ID
- PROMISE / 202504919
- Conditions
- Adverse Childhood Experience, Endothelial Function (FMD), Endothelial Injury, Mitochondrial Function, Oxidative Stress, Psychosocial Influence on Cardiovascular Disease
- Keywords
- flow mediated dilation, mitoquinone mesylate, placebo, early life adversity, trier social stress test
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 300 participants (estimated)
- Lead sponsor
- University of IowaUniversity, hospital or other
- Collaborators
- MitoQ Limited
- Study start
- 13 Oct 2025 (actual)
- Primary completion
- 31 Jul 2026 (estimated)
- Study completion
- 31 Dec 2026 (estimated)
- First posted
- 24 Nov 2025 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. Greater exposure to ACEs are associated with greater increases in the risk of cardiovascular diseases and death. Our laboratory has previously observed that vascular function is disrupted in young adults with prior ACE exposure, even though these individuals appear to be healthy clinically (i.e., no classic clinical cardiovascular disease risk factors). There is a need to identify and understand the biological mechanisms underlying these vascular impairments to inform effective interventions to reduce cardiovascular risks the millions of individuals affected by ACEs.
The body's response to stress is coordinated across various systems, all of which depend on energy supplied by mitochondria (often referred to as the "powerhouse of cells"). Based on new evidence across multiple physiological systems from our team, our overarching hypothesis is that disruption of mitochondrial function contributes to cardiovascular impairments among young adults with ACEs. Here we propose the initial pilot work necessary to begin to understand these associations, which will directly inform identification of individuals who may be most vulnerable to stress-related cardiovascular risk and the development of interventions to promote cardiovascular-stress resilience.
Our aims are to:
- Determine whether mitochondrial oxidative stress contributes to impaired vascular function among young adults who experienced early life adversity.
- Determine whether reducing mitochondrial oxidative stress improves the cellular stress and integrated cardiovascular response to laboratory-based psychosocial stress among young adults who experienced early life adversity.
Detailed description
Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. ACEs promote cardiovascular morbidity and mortality in a graded, dose-dependent manner1 and are thus a significant, widespread determinant of cardiovascular disease (CVD). In agreement with preclinical evidence,2 we have established that young adults (18-29 y) with prior ACE exposure exhibit impaired vascular endothelial function (VEF)3 as evidenced by reduced flow mediated dilation even in the absence of clinical CVD risk factors. The vascular endothelium is a regulatory organ that plays a critical role in maintaining cardiovascular homeostasis, and our findings indicate that vascular endothelial dysfunction is one of the earliest identifiable pathophysiological mechanisms linking ACE exposure with future CVD. There remains a critical biomedical need to identify and understand the psychobiological mechanisms underlying ACEs-related vascular endothelial dysfunction to inform effective interventions to improve cardiovascular health in the millions of individuals affected by ACEs. The physiologic response to stress is coordinated across various physiological systems, all of which depend on energy supplied at the cellular level by mitochondria. Based on novel evidence across multiple physiological systems from our team, our overarching hypothesis is that dysregulation of mitochondrial function due to chronic stress burden - or mitochondrial allostatic load (MAL) - promotes dysregulation of the physiological stress response which is ultimately transduced to impairments in VEF in young adults with ACEs. Notably, our preliminary evidence also suggests that psychological resilience and executive functions such as cognitive reappraisal may moderate these relations, reducing MAL and preserving VEF in the face of substantial adversity. Here we propose the critical work necessary to understand these associations, which will directly inform identification of individuals who may be most vulnerable to stress-related cardiovascular risk and the development of interventions to promote cardiovascular-stress resilience.
In this study, we will use an acute dose of a mitochondrial targeted antioxidant supplement (MitoQ; or placebo) to experimentally interrogate the role of mitochondrial oxidative stress is associated with improvements in 1) vascular endothelial function and 2) cellular and integrated cardiovascular responses to a standardized laboratory based psychosocial stressor in young adults with Adverse Childhood Experiences.
Participants will report to the laboratory, provide a blood sample and have vascular endothelial function assessed using a specialized test known as flow mediated dilation, consume a single acute dose of MitoQ previously demonstrated to be effective and safe for acutely decreasing mitochondrial oxidative stress in humans OR placebo, and then have vascular endothelial function measured again. Next, participants will provide another blood sample before undergoing a standardized and commonly used laboratory psychosocial stress test known, before providing additional blood samples after test completion.
- Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The adverse childhood experiences (ace) study. American Journal of Preventive Medicine. 1998;14:245-58. 2. Su S, Jimenez MP, Roberts CT, Loucks EB. The role of adverse childhood experiences in cardiovascular disease risk: A review with emphasis on plausible mechanisms. Curr Cardiol Rep. 2015;17:88. PMC4941633 3. Jenkins NDM, Rogers EM, Banks NF, Tomko PM, Sciarrillo CM, Emerson SR, Taylor A, et al. Childhood psychosocial stress is linked with impaired vascular endothelial function, lower sirt1, and oxidative stress in young adulthood. Am J Physiol Heart Circ Physiol. 2021;321:H532-H41. PMC8461842
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, investigator, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Mitoquinone Mesylate (MitoQ) | Experimental | Dietary Supplement: Mitoquinone mesylate (MitoQ)Mitoquinone Mesylate (160 mg, single dose) |
| Placebo | Placebo comparator | Dietary Supplement: PlaceboMatched placebo (microcrystalline cellulose and tapioca, 160 mg, single dose) |
Who may qualify
- Ages
- 18 to 29 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (2 listed)
- 18-29 years
- ACE score >=4
Key exclusion criteria (12 listed)
- Resting arterial blood pressure >140/90 mmHg
- BMI <=17 or >= 35
- Are on a weight-loss diet or involved in a formal weight-loss program or are not intentionally weight stable for 6 months (+/- 5 kg) prior to the study.
- Cardiovascular or metabolic prescription drug use
- Vasoactive antidepressant drug use (SSRIs and clonidine)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Mitoquinone mesylate (MitoQ)Participants will consume a single 160 mg dose of mitoquinone mesylate, provided in the form of 6, 20 mg capsules, with water. | Dietary supplement | Mitoquinone Mesylate (MitoQ) |
| PlaceboParticipants will consume a single 160 mg dose of microcrystalline cellulose and tapioca (placebo), provided in 20 mg capsules, with water. | Dietary supplement | Placebo |
Primary outcome
Vascular endothelial function
Time frame: Prior to supplementation and 60 minutes after supplementation
Vascular endothelial function will be assessed using the brachial artery flow mediated dilation technique
Blood pressure
Time frame: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
The blood pressure response to psychosocial stress induced by the Trier Social Stress Test will be determined using beat-to-beat blood pressure measurement by finger photoplethysmography (or brachial artery blood pressure in the case of equipment errors). The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Endothelial Cell Microparticle Release
Time frame: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 min following the Trier Social Stress Test.
Endothelial cell microparticle release will be quantified from platelet-poor plasma in response to psychosocial stress induced by the Trier Social Stress Test. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
Cortisol
Time frame: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 min following the Trier Social Stress Test.
Cortisol will be quantified from drool collected passively to assess the HPA-axis response to psychosocial stress induced by the Trier Social Stress Test. The Trier Social Stress Test will be performed after post-supplementation measurement of vascular endothelial function (FMD).
3 secondary outcomes
Total Peripheral Resistance
Time frame: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
Cardiac Output
Time frame: 75 minutes after supplementation, during, and for 45 minutes after completion of the Trier Social Stress Test.
Growth Differentiation Factor 15
Time frame: 60 minutes after supplementation and immediately following, 5-10 min, 15-20 min, and 45 minutes after completion of the Trier Social Stress Test.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Nov 2025.
- Background: PubMed 34328346Jenkins NDM, Rogers EM, Banks NF, Tomko PM, Sciarrillo CM, Emerson SR, Taylor A, Teague TK. Childhood psychosocial stress is linked with impaired vascular endothelial function, lower SIRT1, and oxidative stress in young adulthood. Am J Physiol Heart Circ Physiol. 2021 Sep 1;321(3):H532-H541. doi: 10.1152/ajpheart.00123.2021. Epub 2021 Jul 30.
- Background: PubMed 26289252Su S, Jimenez MP, Roberts CT, Loucks EB. The role of adverse childhood experiences in cardiovascular disease risk: a review with emphasis on plausible mechanisms. Curr Cardiol Rep. 2015 Oct;17(10):88. doi: 10.1007/s11886-015-0645-1.
- Background: PubMed 9635069Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, Marks JS. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998 May;14(4):245-58. doi: 10.1016/s0749-3797(98)00017-8.
- Individual participant dataSharing planned: Undecided
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Mitoquinone mesylate (MitoQ) in people with Adverse Childhood Experience and Endothelial Function (FMD), run by University of Iowa at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 12 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 24 Nov 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Manoela Lima Oliveria, PhD ((319)467-3125, manoela-limaoliveira@uiowa.edu), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Vascular endothelial function (time frame: Prior to supplementation and 60 minutes after supplementation). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT07244809, which also lists 3 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 24 Nov 2025.