ArticleNature communications2023
Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial Ca
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- PGC-1α pathway dysregulation disrupts myofiber specification in a mouse model of SBMA.JCI insight · 2026Article
- BCL6 regulates skeletal muscle mass and mitochondrial bioenergetics.Molecular metabolism · 2026Article
- Neuromuscular Mechanisms and Oxidative Stress in Skeletal Muscle Atrophy: Emerging Stem Cell and Gene-Based Therapeutic Strategies.Muscles (Basel, Switzerland) · 2026Review
- Review
- Mitochondrial Metabolomics in Cancer: Mass Spectrometry-Based Approaches for Metabolic Rewiring Analysis and Therapeutic Discovery.Metabolites · 2025Review
- Kv3 channel agonist ameliorates the phenotype of a mouse model of amyotrophic lateral sclerosis.Acta neuropathologica communications · 2025Article
- Neuromuscular junction transcriptome analysis of spinal and bulbar muscular atrophy mice implicates sarcomere gene expression and calcium flux dysregulation in disease pathogenesis.Human molecular genetics · 2025Article
- Dysregulated synaptic gene expression in oligodendrocytes of spinal and bulbar muscular atrophy.JCI insight · 2025Article
- Micro-Doses of DNP Preserve Motor and Muscle Function with a Period of Functional Recovery in Amyotrophic Lateral Sclerosis Mice.Annals of neurology · 2025Article
- The Role of Insulin Within the Socio-Psycho-Biological Framework in Type 2 Diabetes-A Perspective from Psychoneuroimmunology.Biomedicines · 2024Review
- Differentially disrupted spinal cord and muscle energy metabolism in spinal and bulbar muscular atrophy.JCI insight · 2024Article
- Exercise attenuates polyglutamine-mediated neuromuscular degeneration in a mouse model of spinal and bulbar muscular atrophy.Journal of cachexia, sarcopenia and muscle · 2024Article
- Skeletal muscle in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2023Review
- The Role of Mitochondria in Mediation of Skeletal Muscle Repair.Muscles (Basel, Switzerland) · 2023Review
- LSD1/PRMT6-targeting gene therapy to attenuate androgen receptor toxic gain-of-function ameliorates spinobulbar muscular atrophy phenotypes in flies and mice.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 6 institutions in 2 countries.
Funding
Abstract
Polyglutamine expansion in the androgen receptor (AR) causes spinobulbar muscular atrophy (SBMA). Skeletal muscle is a primary site of toxicity; however, the current understanding of the early pathological processes that occur and how they unfold during disease progression remains limited. Using transgenic and knock-in mice and patient-derived muscle biopsies, we show that SBMA mice in the presymptomatic stage develop a respiratory defect matching defective expression of genes involved in excitation-contraction coupling (ECC), altered contraction dynamics, and increased fatigue. These processes are followed by stimulus-dependent accumulation of calcium into mitochondria and structural disorganization of the muscle triads. Deregulation of expression of ECC genes is concomitant with sexual maturity and androgen raise in the serum. Consistent with the androgen-dependent nature of these alterations, surgical castration and AR silencing alleviate the early and late pathological processes. These observations show that ECC deregulation and defective mitochondrial respiration are early but reversible events followed by altered muscle force, calcium dyshomeostasis, and dismantling of triad structure.
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.