ArticleHeliyon2024
Modelling energy metabolism dysregulations in neuromuscular diseases: A case study of calpainopathy.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
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Who cites it
2 citing papers in PubMed.
- Distributed Pharmacodynamic Architecture in Multi-Component Herbal Formulations: A Flux-Based Framework for Redox-Heterogeneous Diseases.Pharmaceutics · 2026Review
- Redox-Guided Epigenetic Signaling in Cancer: miRNA-DNMT Feedback Loops as Epigenetic Memory Modulates.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biological modelling helps understanding complex processes, like energy metabolism, by predicting pathway compensations and equilibrium under given conditions. When deciphering metabolic adaptations, traditional experiments face challenges due to numerous enzymatic activities, needing modelling to anticipate pathway behaviours and orientate research. This paper aims to implement a constraint-based modelling method of muscular energy metabolism, adaptable to individual situations, energy demands, and complex disease-specific metabolic alterations like muscular dystrophy calpainopathy. Our calpainopathy-like model not only confirms the ATP production defect under increasing energy demands, but suggests compensatory mechanisms through anaerobic glycolysis. However, excessive glycolysis indicates a need to enhance mitochondrial respiration, preventing excess lactate production common in several diseases. Our model suggests that moderate-intensity physiotherapy, known to improve aerobic performance and anaerobic buffering, combined with increased carbohydrate and amino acid sources, could be a potent therapeutic approach for calpainopathy.
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Registered trials
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