ArticleCell reports2017
ATP Citrate Lyase Regulates Myofiber Differentiation and Increases Regeneration by Altering Histone Acetylation.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 70 citations in OpenAlex.
- Histone modifications across cancers: mechanisms, therapy and clinical translation.Molecular cancer · 2026Review
- P4HA3 drives cervical cancer lymphatic metastasis by facilitating ACLY-mediated ferroptosis resistance.Cell death and differentiation · 2026Article
- Mitonuclear Communication in Stem Cell Function.Cell proliferation · 2025Review
- Mitochondria - the CEO of the cell.Journal of cell science · 2025Review
- Review
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- The oxygen level in air directs airway epithelial cell differentiation by controlling mitochondrial citrate export.Science advances · 2025Article
- New mechanistic insights into macrophage extracellular trap formation induced by a parasitic nematode,Frontiers in immunology · 2025Article
- Hydroxycitrate delays early mortality in mice and promotes muscle regeneration while inducing a rich hepatic energetic status.Aging cell · 2024Article
- Mitochondrial regulation in stem cells.Trends in cell biology · 2024Review
- Extracellular C1qbp inhibits myogenesis by suppressing NFATc1.Scientific reports · 2024Article
- Psat1-generated α-ketoglutarate and glutamine promote muscle stem cell activation and regeneration.Genes & development · 2024Article
- Metabolic regulation of the hallmarks of stem cell biology.Cell stem cell · 2024Review
- Emerging roles of mitochondrial functions and epigenetic changes in the modulation of stem cell fate.Cellular and molecular life sciences : CMLS · 2024Review
- Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Genetic deletion of skeletal muscle iPLAiScience · 2023Article
- ACL and HAT1 form a nuclear module to acetylate histone H4K5 and promote cell proliferation.Nature communications · 2023Article
- Cancer cachexia: molecular mechanisms and treatment strategies.Journal of hematology & oncology · 2023Review
- Article
- The metabolic recovery of marathon runners: an untargetedFrontiers in physiology · 2023Article
Corrections and comments
- Commented on by
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATP citrate lyase (ACL) plays a key role in regulating mitochondrial function, as well as glucose and lipid metabolism in skeletal muscle. We report here that ACL silencing impairs myoblast and satellite cell (SC) differentiation, and it is accompanied by a decrease in fast myosin heavy chain isoforms and MYOD. Conversely, overexpression of ACL enhances MYOD levels and promotes myogenesis. Myogenesis is dependent on transcriptional but also other mechanisms. We show that ACL regulates the net amount of acetyl groups available, leading to alterations in acetylation of H3(K9/14) and H3(K27) at the MYOD locus, thus increasing MYOD expression. ACL overexpression in murine skeletal muscle leads to improved regeneration after cardiotoxin-mediated damage. Thus, our findings suggest a mechanism for regulating SC differentiation and enhancing regeneration, which might be exploited for devising therapeutic approaches for treating skeletal muscle disease.
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.