ArticleNpj biological timing and sleep2025
Social jetlag alters markers of exercise-induced mitochondrial adaptations in the heart.
Article in Npj biological timing and sleep, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Social jet lag is associated with incident cardiovascular disease independent of sleep duration and cardiac genetic risk.Journal of internal medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Social jetlag (SJL) represents the behavioral misalignment of sleep and wake times on work days and free days, and potently disrupts the circadian rhythm. SJL affects up to 70% of the population worldwide and is associated with increased risk for many cardiometabolic diseases. Animal models of acute SJL have shown disruption in locomotor activity and expression of clock genes in select tissues, its impact on the heart remains unclear. The purpose of this study was to investigate the effects of prolonged SJL (6 weeks), on activity rhythms, and the impact on exercise-induced adaptations in the heart. Male mice (n = 40, C57BL6) were assigned to a control light:dark (LD) cycle or SJL schedule (4-hour shift on weekends) for 6 weeks. Mice in each condition were further divided into voluntary exercise (EX) or sedentary (SED) groups. SJL resulted in significant shifts in the onset of physical activity in both sedentary (SJL-SED) and exercised (SJL-EX) mice on weekends, and exercise accelerated the speed of re-entrainment to the weekday schedule. Exercise induced myocardial hypertrophy in both CON-EX and SJL-EX groups. While there were no changes in mitochondrial content, SJL decreased expression of mitochondrial fusion proteins MFN1 and OPA1, and inhibited exercise-induced increases in MFN2. Taken together, these findings suggest that exercise hastens re-entrainment to the weekday schedule under SJL, but that SJL disrupts exercise-induced alterations to mitochondrial fusion/fission dynamics in the heart. Further investigation of cardiovascular function is warranted and will enable the development of strategies to prevent the effects of SJL on the heart.
Identifiers
What OpenQuestion holds
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.