Evidence map›Paper›PMID 42806210›Full record

ReviewGeroScience2026

Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.

Siyun Kim, Sung Gi Noh, Minje Ji, Kai Chen, George A Kuchel, Iman M Al-Naggar, Oh Sung Kwon

Abstract readReview
PubMed Publisher
In one paragraph

Review in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Siyun KimDepartment of Kinesiology, University of Connecticut, Storrs, CT, USA.
Sung Gi NohDepartment of Kinesiology, University of Connecticut, Storrs, CT, USA.
Minje JiDepartment of Kinesiology, University of Connecticut, Storrs, CT, USA.
Kai ChenUMass Chan Medical School, Worcester, MA, USA.
George A KuchelUConn Center on Aging, UConn Health, Farmington, CT, USA.
Iman M Al-NaggarUConn Center on Aging, UConn Health, Farmington, CT, USA.
Oh Sung KwonDepartment of Kinesiology, University of Connecticut, Storrs, CT, USA. ohsung.kwon@uconn.edu.ORCID http://orcid.org/0000-0003-2935-1130

Funding

The Mito-Frail Trial: Effects of MitoQ on Vasodilation, Mobility and Cognitive Performance in Frail Older AdultsK01AG080164 · NIA · UNIVERSITY OF CONNECTICUT STORRS · PI Oh Sung Kwon · 2023 to 2026
$538k
NIA NIH HHS K01AG080164UConn Claude D. Pepper Older Americans Independence Center P30AG067988
6 · The paper itself

Abstract

Aging is an inevitable and progressive physiological process marked by a decline in cellular function, accumulation of somatic mutations, decreased ability to maintain homeostasis, and increased tissue and organ dysfunction. These changes contribute to the onset and progression of various age-related diseases. Accumulation of reactive oxygen species (ROS) has been identified as a key mediator of the aging process. Mitochondria, the primary producers of ROS, accumulate defects with aging, leading to increased mitochondrial oxidative stress. These defective mitochondria are both a source and a target of oxidative stress, creating a vicious cycle that accelerates aging and the progression of age-related diseases. Consequently, targeting mitochondria represents a promising therapeutic approach to prevent aging-related physiological dysfunction. MitoQ, a mitochondria-targeted antioxidant, has been extensively studied due to its ability to effectively scavenge mitochondria-derived ROS, owing to its lipophilic cation properties. This review explores the effects of MitoQ on aging-associated physiological dysfunction, specifically exploring its impact on cardiovascular, neuronal, and skeletal muscle functions. By addressing the central role of mitochondrial oxidative stress, we propose that MitoQ represents a promising strategy to counteract aging-associated physiological dysfunction.

Indexed as

Age-related diseaseAgingMitochondria-derived ROSMitochondria-targeted antioxidantsMitoQOxidative stress

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.