ArticleCommunications medicine2026
Skeletal muscle transcriptional dysregulation of genes involved in senescence is associated with prognosis in severe heart failure.
Article in Communications medicine, 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.
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Who cites it
1 citing paper in PubMed.
- Multi-Omics Epigenetic Landscape Unveils Regulatory Mechanisms Underlying Heterosis in Sheep Muscle Development.Animals : an open access journal from MDPI · 2026Article
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Authors and funding
5 authors.
Funding
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Abstract
backgroundThe skeletal muscle hypothesis refers to a vicious cycle of successive deterioration of left ventricular function, skeletal muscle remodeling, and functional capacity in patients with heart failure. Despite extensive research, the regulatory mechanisms and their associations with clinical status and prognosis are still largely unclear.
methodsTo identify mechanisms and characterize underlying processes involved in the disease pathophysiology, we performed RNA sequencing and network analysis using human skeletal muscle samples from 58 patients with severe symptomatic heart failure. A co-expression network with communities involved in established biological processes within human skeletal muscle was identified and validated in two independent cohorts.
resultsHere, we show network communities associated with mitochondrial beta-oxidation, extracellular matrix remodeling, oxidative phosphorylation, and contractile elements with lower expression in heart failure patients than in age-matched controls. Based on the strong correlation with clinical features and prognosis, extracellular matrix remodeling, mitochondrial beta-oxidation, and p53 signalling communities are identified as key underlying processes. The former two communities are highly enriched with genes regulated by physical (in)activity, i.e., bed rest and exercise, and associated weakly with prognosis. Community related to p53 signalling, with CDKN1A as a key regulator, is increased in heart failure patients relative to age-matched controls and associated with worse prognosis.
conclusionThe current work differentiates previously proposed factors underlying heart failure-induced skeletal muscle dysfunction, emphasizing the p53 signalling community and importance of biological age in this process. The distinct association with clinical status and prognosis furthermore supports pathophysiological significance and clinical potential of this community.
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