Trial reportPloS one2026
Transcriptomic response of skeletal muscle to acute aerobic versus combined exercise in chronic kidney disease.
Trial report in PloS one, 2026. 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
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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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic kidney disease (CKD) affects approximately 14% of the UK population and is associated with significant exercise intolerance, partly due to skeletal muscle dysfunction. While exercise is a potential therapeutic strategy, the molecular response of skeletal muscle to exercise in CKD remains poorly understood. This study aimed to characterise transcriptomic changes in skeletal muscle 24 hours after aerobic (AE) or combined aerobic and resistance exercise (CE) in non-dialysis CKD.
methodsThis study utilised muscle biopsies from participants in the ExTRA CKD trial with stage 3b-4 CKD stages 3b-4 (AE: 24 (15-32) ml/min/1.73m2; CE: 25 (19-31) ml/min/1.73m2). Participants (n = 4 per group) were randomised to 12 weeks of thrice-weekly AE or CE. Vastus lateralis skeletal muscle biopsies were collected at baseline and 24h after the first bout of exercise. RNA was extracted for Bulk RNA sequencing. Bulk RNA sequencing was performed, and differentially expressed genes (DEGs) were identified between baseline and post-exercise samples, followed by pathway enrichment analysis.
resultsFollowing AE, 1480 genes were upregulated and 1554 downregulated. CE resulted in 556 upregulated and 115 downregulated genes. The most upregulated gene after AE was CHI3L1 (log₂FC 10.7), followed by SAA2 and PTX3, all associated with inflammation. After CE, SFN (log₂FC 6.8) and MT1A were among the most highly upregulated. Enrichment analysis showed strong activation of inflammatory and cellular senescence pathways, and downregulation of mitochondrial function-related processes, particularly after AE.
conclusionBoth AE and CE triggered robust inflammatory gene expression responses in CKD skeletal muscle, which may be indicative of early repair processes. Unexpectedly, mitochondrial-related pathways were downregulated at 24h post exercise. In the absence of earlier post exercise timepoints, it is not possible to determine whether these findings reflect impaired mitochondrial adaptation, or instead represent a recovery phase return of mitochondrial gene expression levels to baseline. These results highlight mitochondrial dysfunction may be a potential barrier to effective exercise adaptation and a possible therapeutic target in this population.
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