ArticleCommunications biology2023
Downregulation of mitochondrial metabolism is a driver for fast skeletal muscle loss during mouse aging.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 12 citations in OpenAlex.
- A positively selected microRNA controls a reversible aging program in striated muscle.bioRxiv : the preprint server for biology · 2026Article
- Vitamin B12 improves skeletal muscle mitochondrial biology in aged mice.GeroScience · 2026Article
- Ghrelin Receptor Deletion or Pharmacological Inhibition Improves Muscle Function in Aging Male Mice.Aging cell · 2026Article
- Transcriptomic and epigenetic alterations in aging-related genes in the medaka liver due to ancestral BPA exposure.Journal of the Endocrine Society · 2026Article
- The Axon as a Self-Modifying Computational System: Autonomous Inference, Adaptive Propagation, and AI-Enabled Mechanistic Insight.International journal of molecular sciences · 2026Review
- Musculoskeletal biomarkers in health and disease: implications for the aging spine-a review for spinal surgeons by the SRS adult spinal deformity task force on senescence.Spine deformity · 2025Review
- Ultrasound irradiation activates purine metabolism and mitochondrial respiration via the MAPK signaling pathway in myotubes.Biochemistry and biophysics reports · 2025Article
- Circulating small extracellular vesicles as blood-based biomarkers of muscle health in aging nonhuman primates.GeroScience · 2025Article
- Methylome-proteome integration after late-life voluntary exercise training reveals regulation and target information for improved skeletal muscle health.The Journal of physiology · 2025Article
- HomozygousMolecular genetics and metabolism reports · 2024Article
- Mouse sarcopenia model reveals sex- and age-specific differences in phenotypic and molecular characteristics.The Journal of clinical investigation · 2024Article
- Dysfunctional mitochondria elicit bioenergetic decline in the aged heart.The journal of cardiovascular aging · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle aging is characterized by the loss of muscle mass, strength and function, mainly attributed to the atrophy of glycolytic fibers. Underlying mechanisms driving the skeletal muscle functional impairment are yet to be elucidated. To unbiasedly uncover its molecular mechanisms, we recurred to gene expression and metabolite profiling in a glycolytic muscle, Extensor digitorum longus (EDL), from young and aged C57BL/6JRj mice. Employing multi-omics approaches we found that the main age-related changes are connected to mitochondria, exhibiting a downregulation in mitochondrial processes. Consistent is the altered mitochondrial morphology. We further compared our mouse EDL aging signature with human data from the GTEx database, reinforcing the idea that our model may recapitulate muscle loss in humans. We are able to show that age-related mitochondrial downregulation is likely to be detrimental, as gene expression signatures from commonly used lifespan extending interventions displayed the opposite direction compared to our EDL aging signature.
Indexed as
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.