ReviewiMetaOmics2026
Move beyond free radical theory of aging.
Review in iMetaOmics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a gradual pathophysiological process with the loss of functional integrity and gain of disease vulnerability. Mitochondrial DNA is one essential regulatory factor of aging. The canonical free radical theory attributes aging to oxidative damage of mitochondrial DNA caused by free radicals. However, the general validity of this theory has been challenged by incremental evidences, including some seemingly paradoxical reports, which motivates us to substantiate this theory with our current understandings on free radicals and aging. After reviewing this canonical theory and its adapted models, we provided updated insights by emphasizing the dosage-dependent dual roles of free radicals played during aging and characterizing adenosine 5'-monophosphate-activated protein kinase as the nexus between mitochondrial health and free radicals. For practical use, we provided detailed recommendations regarding the dosages of reactive species feasible for treating different health concerns. Additionally, we proposed cold atmospheric plasma (CAP), which is composed of a cocktail of free radicals, as an innovative redox modulatory tool for anti-aging if used appropriately, alone or in combination with other interventions. Our view not only centers mitochondrial redox disequilibrium in the progression of aging, but also underpins the essential value of the fourth state of matter as represented by CAP in keeping redox homeostasis for the sake of human health that should be appropriately harnessed.
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Registered trials
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.