NCT07244809: PROMISE

Probing the Role of Mitochondrial Oxidative Stress in Impaired Vascular Function Among Young Adults With Early Life Adversity

Recruiting now NA Last updated 24 November 2025

What this trial tests

NA trial testing Mitoquinone mesylate (MitoQ) in Adverse Childhood Experience in 300 participants. Currently enrolling.

Timeline

13 October 2025

Primary endpoint
31 July 2026

31 December 2026

Quick facts

Lead sponsor	University of Iowa
Phase	NA
Status	Recruiting now
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	triple
Primary purpose	basic science
Enrollment	300
Start date	13 October 2025
Primary completion	31 July 2026
Estimated completion	31 December 2026
Sites	1 location across United States

Drugs / interventions tested

• Mitoquinone mesylate (MitoQ) — full drug profile →
• Placebo

Conditions studied

• Adverse Childhood Experience — all drugs for Adverse Childhood Experience →
• Endothelial Function (FMD) — all drugs for Endothelial Function (FMD) →
• Endothelial Injury — all drugs for Endothelial Injury →
• Mitochondrial Function — all drugs for Mitochondrial Function →

Sponsor

University of Iowa

Who can join

Adults 18 to 29, any sex, with Adverse Childhood Experience or Endothelial Function (FMD). Patients with the condition only — healthy volunteers not accepted.

Sponsor's own 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. 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:

1. Determine whether mitochondrial oxidative stress contributes to impaired vascular function among young adults who experienced early life adversity.
2. 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.

Publications & conference data

No peer-reviewed publications indexed yet for this trial.