ArticleJournal of molecular cell biology2015
HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth.
Article in Journal of molecular cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
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- Exploring the Role of Oleic Acid in Muscle Cell Differentiation: Mechanisms and Implications for Myogenesis and Metabolic Regulation in C2C12 Myoblasts.Biomedicines · 2025Article
- The Spatial-Temporal Alternative Splicing Profile Reveals the Functional Diversity of FXR1 Isoforms in Myogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Candidate circRNAs related to skeletal muscle development in Dazu black goats.Animal biotechnology · 2024Article
- Aligning with the 3Rs: alternative models for research into muscle development and inherited myopathies.BMC veterinary research · 2024Review
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- Fatty acids metabolism affects the therapeutic effect of anti-PD-1/PD-L1 in tumor immune microenvironment in clear cell renal cell carcinoma.Journal of translational medicine · 2023Article
- Hacd2 deficiency in mice leads to an early and lethal mitochondrial disease.Molecular metabolism · 2023Article
- Correlation between Mild Cognitive Impairment and Sarcopenia: The Prospective Role of Lipids and Basal Metabolic Rate in the Link.Nutrients · 2022Article
- Synergistic Effects of Multiple Factors Involved in COVID-19-dependent Muscle Loss.Aging and disease · 2022Article
- Defining and identifying satellite cell-opathies within muscular dystrophies and myopathies.Experimental cell research · 2022Article
- Phospholipids: Identification and Implication in Muscle Pathophysiology.International journal of molecular sciences · 2021Review
- Cardiolipin content controls mitochondrial coupling and energetic efficiency in muscle.Science advances · 2021Article
- Differential physiological roles for BIN1 isoforms in skeletal muscle development, function and regeneration.Disease models & mechanisms · 2020Article
- FABP3-mediated membrane lipid saturation alters fluidity and induces ER stress in skeletal muscle with aging.Nature communications · 2020Article
- Biallelic LINE insertion mutation inNeurology. Genetics · 2020Article
- Update on Congenital Myopathies in Adulthood.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
22 authors at 8 institutions in 3 countries.
Funding
Abstract
The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demonstrate that in normal differentiating myoblasts, expression of the catalytically active HACD1 isoform, which is encoded by a muscle-enriched splice variant, yields decreased lysophosphatidylcholine content, a potent inhibitor of myoblast fusion, and increased concentrations of ≥ C18 and monounsaturated fatty acids of phospholipids. These lipid modifications correlate with a reduction in plasma membrane rigidity. In conclusion, we propose that fusion impairment constitutes a novel, non-exclusive pathological mechanism operating in congenital myopathies and reveal that HACD1 is a key regulator of a lipid-dependent muscle fibre growth mechanism.
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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.